10857757
Description
Flashcards by Harry Robertson, updated more than 1 year ago
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Created by Harry Robertson
over 6 years ago
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| Question | Answer |
| What is the most worrying complication of sinusitis and occurs most commonly in children? | Periorbital cellulitis, can cause blindness |
| Describe chandler's classification of periorbital cellulitis | Used to communicate severity I) pre-septal cellulitis - confined to eyelid i.e anterior to superior orbital septum II) orbital cellulitis without abscess - cellulitis involving the orbit III) orbital cellulitis with periosteal abscess - cellulitis with abscess confined to the orbital periosteum IV) Intra-orbital abscess V) cavernous sinus thrombosis |
| Describe the A to E approach in a patient who is acutely unwell | A - airway B - breathing C - circulation |
| What is given to a patient who has had an opioid overdose? | Naloxone |
| Describe what signs you would see in a patient with sepsis and what approach you take | -Raised RR, HR and temp -Acidosis and pain Sepsis 6 - take 3 - cultures, urine output, measure serum lactate and a full blood count -Give 3 - oxygen, fluids, broad spectrum Abx |
| What is seen in a patient with peritonitis on examination? | Guarding, rebound tenderness |
| What is given in acute asthma? | MgSO4, ipratropium bromide, steroids, salbutamol |
| Why may a normal CO2 value be misleading and potentially serious in a patient suffering from a severe asthma attack | Would expect CO2 to be low as patient is hyperventilating therefore blowing off lots of CO2. If it is normal, this shows that CO2 is being retained and patient is beginning to get tired and enter respiratory failure. This is very serious. |
| What are the complications of sinusitis? | Meningitis, periorbital sinusitis, cavernous sinus thrombosis. |
| What is trismus? | Quinsy that begins to affect the pterygoid muscle meaning patient is unable to open mouth. |
| What are the three main differentials of a midline neck lump and how can you quickly distinguish between them? | Thyroid lump, thyroglossal cyst, dermoid. Thyroid lump will not move when protruding the tongue. |
| What is a cholesteatoma? | A destructive and expanding growth consisting of keratinizing squamous epithelium in the middle ear and/or mastoid process |
| What kind of weakness is described in a patient with NMJ problems? | Fatiguable weakness |
| Describe the set of signs in a patient with cerebellar problems? | D- Dysdiadochokinesis A - ataxia N - nystagmus I - intention tremor S - slurred speech H - hypotonia P - past pointing |
| What is the first line treatment of rhinosinusitis? | Topical drugs with steroids, antihistamines, anticholinergics (actually rarely used), decogestants |
| What are the surgical options in a patient with rhinosinusitis? | SMD - submucous diathermy, polypectomy if present, FESS (functional endoscopic sinus surgery) |
| Describe the staging of haemorrhage in terms of blood loss, response and treatment | class I - <15% loss, minimal fast heart rate, normal BP Class II - 15-30% loss, fast HR, minimal low blood pressure, IV fluids Class III - 30-40%, very fast HR, low blood pressure, confusion Class IV - >40%, critical BP and HR, aggressive interventions. |
| What is little's area? | Area in the nose where 4 arteries anastomose to form Kiesselbach's plexus. Made up of the anterior ethmoidal, sphenopalatine, greater palatine and septal branch of the superior labial arteries. |
| What are the surgical options for epistaxis? | -Sphenopalatine artery ligation -Anterior ethmoidal artery ligation (mainly done following trauma) -External carotid artery ligation (very rarely done) |
| What is leukoplakia? | White patch in the mouth that cannot be removed by rubbish. Closely linked to an increased risk of mouth cancer. |
| 5 main risk factors for head and neck cancer | -Smoking -Spirits -Spices (betel nut) -Age -HPV |
| What is the alternative name for a pharyngeal pouch and what are the main presenting complaints? | Zenker's diverticulum. -Dysphagia -Halitosis -risk of aspiration -regurg -cough |
| What is sarcoidosis? | Disease involving abnormal collections of inflammatory lumps known as granulomas |
| What is hepatopulmonary syndrome and what is it's pathogenesis? | Syndrome of shortness of breath and hypoxaemia caused by formation of microscopic arteriovenous vasodilations. This causes over perfusion of the lungs relative to ventilation causing a V/Q mismatch. |
| What is carbocisteine? | Mucolytic that reduces that viscosity of sputum |
| Why do you not cauterise epsitaxis on both sides? | Risk of causing cartilagenous necrosis and subsequent septal perforation |
| What is an important consideration when administering naseptin? | Contains peanut oil therefore essential to check for allergies. |
| Which test can be used to determine whether a fluid is CSF? | beta 2 transferrin test |
| Describe the benefits of FNA vs excision biopsy for neck lumps | FNA good for looking for SCC, if comes back negative can progress to excision biopsy. Excision biopsy good for looking for lymphoma and TB. |
| What are the 5 T's of referred ear pain? | -Teeth -TMJ -Tonsils -Thyroid -Throat |
| What is an important consideration in a patient with bacterial tonsilitis with a differential of glandular fever? | Do not give amoxicillin because causes rash in glandular fever. |
| What is hot potato voice a sign of? | Quinsy |
| What is important to do in a patient with epiglotitis? | Do not antagonise or do anything patient because can cause epiglottis to completely shut and air way lost. |
| What is steakhouse syndrome and how serious is it? | Oesophageal food bolus obstruction. Medical emergency, patients are at risk of oesophageal perforation or aspiration into the trachea. |
| Describe the embryology of the hypothalamus | Part of the forebrain |
| Describe the embryology of the anterior pituitary | Comes from he ectoderm of the primitive mouth (rathke's pouch). It moves upwards to join the infundibulum from the hypothalamus. As its original blood supply is lost, it develops a new one from the hypothalamus. This blood supply is the only connection between the hypothalamus and the anterior pituitary |
| Describe the embryology of the posterior pituitary | Develops from the neuroectoderm and grows down from the hypothalamus. This allows neurosecretory cells to join the hypothalamus and the posterior pituitary, forming their only means of communication. |
| Describe the location of the pituitary and how this is clinically important. How are the posterior pituitary and the hypothalamus connected | Sits in an indentation in the sphenoid bone called the sella tursica, covered by the diaphragma sellae which is a thin piece of fibrous tissue. Lies directly beneath the optic chiasm which means that any large tumours of the pitutiary can press on the chiasm and cause visual disturbances. The [posterior pituitary is connected to the median eminence of the hypothalamus by the infundibulum. |
| Describe the divisions of the anterior pituitary | Pars distalis - main part of the gland Pars intermedia - this lies between the anterior and posterior parts of the gland and consists of the corticotroph cells Pars tuberalis - this surrounds the infundibulum and contains mostly gonadotroph cells. |
| Describe the blood supply/drainage to the hypothalamus and anterior pituitary | From the superior hypophyseal artery. Blood then travels via the portal veins, through the median eminence to the anterior pituitary. It drains into the cavernous sinuses. |
| Describe the blood supply/drainage of the posterior pituitary | Inferior hypophyseal arteries and drains back into the cavernous sinus |
| Describe the connection between the anterior pituitary and the hypothalamus | The anterior pituitary is made up of secretory epithelial tissues and is attached to the hypothalamus by a portal venous blood supply. the hypothalamus releases hormones into these veins and they then stimulate or inhibit the pituitary tissue. When cells of the anterior pituitary are stimulated, they release their hormones into the systemic circulation. |
| Describe the connection between the posterior pituitary and the hypothalamus | The posterior pituitary is made up of neuroendocrine tissue, so although it also derives a blood supply from the hypothalamus, this is not how it received its instructions. Instead, neurosecretory cell axons run from the hypothalamus down to the posterior pituitary. The axon terminals are located next to blood sinusoids and release neurosecretory granules when the cells are stimulated. The cells of the posterior pituitary itself are glial cells that support the axons of cells that originate in the hypothalamus. |
| List the hormones of the hypothalamus, the cells they effect in the anterior pituitary and the effect it has | GHRH - causes somatotrophs to increase GH release GHIH (somatostatin) - causes somatotrophys and thyrotrophs to decrease GH and TSH release CRH - causes corticotrophs to increase ACTH release GnRH - causes gonadotrophs to increase LH and FSH release TRH - Causes thyrotrophs and lactotrophs to increase TSH and prolactin release Prolactin release factors (PRF) - causes lactotrophs to increase prolactin release Dopamine (prolactin inhibiting hormone) - causes lactotrophs to decrease prolactin release |
| Give the first 3 main hormones of the anterior pituitary, what they are produced by (cell type), the effect they have and what stimulates and suppresses them | 1) Growth hormone - produced by somatotrophs to stimulate the liver to produce IGF-1 and oppose action of insulin. Stimulated by GHRH and suppressed by GHIH and IGF-1 2) TSH - produced by thyrotrophs, stiulates the thyroid gland to release thyroxine. Stimulated by TRH and suppressed by T3. 3) ACTH - produced by corticotrophs to stimulate the adrenal cortex to release glucocorticoids, adrenal androgens and aldosterone. Stimulated by CRH and inhibited by glucocorticoids. |
| Give the second 3 main hormones of the anterior pituitary, what they are produced by (cell type), the effect they have and what stimulates and suppresses them | 1) LH and FSH - produced by gonadotrophs, causes the release of sex steroids from the reproductive organs. Stimulated by GnRH and sex steroids and suppressed by prolactin and sex steroids (dependent on concentrations) 2) Prolactin - Produced by lactotrophs, initiates lactation and promotes growth of mammary glands and reproductive organs. Stimulated by PRF and TRH and suppressed by dopamine 3) MSH - produced by corticotrophs, stimulates melanin syntehsis in melanocytes in the skin. |
| What are the two hormones of the posterior pituitary, what are they produced by and what is their effect. what are the stimualted and suppressed by? | 1) ADH - produced by supraoptic vasopressinergic neurons, increases the permeability of the collecting ducts in the kidneys, causing greater reabsorption of water. Stimulated by raised osmolarity and low blood volume, suppressed by reduced osmolarity. 2) Oxytocin - produced by paraventricular oxytocinergic neurons, causes smooth muscle contraction of the uterus (leading to birth) or the mammary glands (leading to milk ejection). Stimulated by stretch receptors in the nipple or cervix and oestrogen, suppressed by stress. |
| What are the 5 main causes and 4 very rare causes of disorders of the hypothalamus and pituitary | 5 main - Idiopathic -Invasion (i.e tumours) -Infarction (e.g sheehans syndrome) -Iatrogenic (surgery, radiotherapy or certain drugs) -Injury Very rare causes -Infection (eg TB) -Infiltration (eg sarcoidosis) -Inherited (eg congenital hormone deficiency) -Immunological (eg lymphocytic hypophysitis) |
| What is sheehan's syndrome? | Also known as postpartum pituitary gland necrosis, is hypopituitarism caused by ischaemic necrosis due to blood loss and hypovolaemic shock during or after childbirth |
| What investigations can be employed to assess disorders of the hypothalamus and the pituitary? | 1) basal blood tests - hormones that are relatively constant in the bloodeg TSH can be measured as a baseline test. This means a blood test can be taken at any time because the results of a healthy individual should always lie in a particular range. Considerations must be taken for time and situation in hormones that fluctuate more (eg GH, ACTH) 2) In cases where basal tests are unclear, it is better to perform dynamic tests. They are either suppression or stimulation tests. If a hormone is stimulated, by levels do not rise, then there must be a problem with the production of the hormone. if an inhibiting substance is given, but normal negative feedback does not occur, then there is likely to be a hormone producing tumour causing the symptoms. 3) if a tumour is suspected, MRI is normally used. |
| What are the three main forms of treatment for disorders of the pituitary and the hypothalamus? | 1) replacement hormones - for deficiency problems or when other treatments designed to reduce excess hormone output destroy too much glandular tissue 2) surgery or radiotherapy - for tumours 3) drugs that inhibit hormone production - when surgery or radiotherapy is not suitable. |
| Describe the test used to assess whether a person has excess GH | Oral glucose tolerance test. Glucose and GH are measured at 30 minute intervals fo 150 minutes. Insulin is released in response to the glucose. In healthy people, insulin causes suppression of GH. However, if there is no suppression or if levels of GH rise, this is diagnostic of acromegaly. |
| What are the treatment options for acromegaly? | 1) surgery 2) radiotherapy 3) suppression of GH with ocreotide (if the patient or tumour is not suitable for surgery or radiotherapy) |
| Why would a person with acromegaly have changes with their vision? | Could potentially be due to a tumour of the pituitary gland pressing on the optic chiasm |
| What is the most common cause of acromegaly and what are the clinical symptoms? between | Functioning somatotroph adenoma that excretes GH. Symptoms - enlarged hands and feet, enlarged skull circumference, enlarged liver, kidneys and heart (predisposes to cardiomyopathy, coarse thickened skin (leads to prominent nasolabial folds and supraorbital ridge), large lower jaw, nose and tongue, spacing between the lower teeth, greasy sweating and temperature intolerance, mental disturbance and insomnia, loss of peripheral vision (compression of the optic chiasm by a tumour), carpal tunnel syndrome |
| Which other conditions are associated with acromegaly? | -1 in 3 have hypertension (predisposes to ischaemic heart disease -1 in 10 are hypercalcaemic -1 in 4 are glucose intolerant (increases risk of developing diabetes -Altered bone structure (predisposes to arthritis) -1 in 5 have hyperthryoidism -Effective treatment of acromegaly is extremely important because high levels of GH over an extended period of time increases the risk of developing malignancy, particularly bowel cancer |
| What screening tests would you perform to confirm a diagnosis of excess cortisol ()? Describe them. | -24 hours urinary free cortisol - determines whether a patient's symptoms are due to increased cortsiol levels. Doing the test over 24 hours means that circadian rhythm does not affect the interpretation. Normal levels should be less than 280nmol/24hr -Overnight dexamethsone suppression test- plasma cortisol is measured and then 1mg dexmethasone is given at midnight. The plasma cortisol is measured again at 8am. This would suppress cortisol levels to less than 50nmol/L in a healthy subject. In patients with excess cortisol, levels will not be suppressed/very little |
| What are the three main causes of cushing's syndrome? Which tests do you perform to work out which it is? | 1) Pituitary adenoma (cushing's disease) producing excess ACTH 2) ectopic ACTH proudction from a tumour (often small cell lung cancer or carcinoid tumour) 3) adrenal adenoma or carcinoma producing excess cortisol First test is a plasma ACTH test - if the problem is hypersecretion from the adrenal glands, the ACTH levels will be suppressed to undectable amounts. If ACTH is normal or high, you need to distinguish between pituitary and ectopic ACTH. Perform a high dose dexamethsone suppression test. if the patient has cushings disease, this will cause at least partial epression of cortisol levels, becuase the exogenous cortsiol will still have some negative feedback effect if the problem is pituitary based. If there is no suppression at high levels, then the source must be ectopic, because these will not have feedback receptors. |
| What is the treatment for cushing's syndrome? | 1) can be treated with surgery 2) iatrogenic causes are treated by removing the source if possible 3) drug therapy using agents such as metyropone or aminoglutethimide to reduce levels of cortisol in the plasma 4) adrenal adenomas/carcinomas are treated with surgical resection, after preparatory treatment with metyropone to reduce the risks of surgery Medical therapy is also used as palliative treatment in cases where malignancy is not resectable. |
| What are the clinical symptomsof cushing's syndrome? | -truncal obesity -supraclavicular fat pad -purple abdominal striae -thin hair/male pattern baldness -Depression, confusion, psychosis, insomnia - moon face (due to facial fat deposition) -acne -hirsutism (coarse pigmented hair growth on the face, chest or abdomen) -Thin, easily bruised skin -Wasting/weakness of skeletal muscle (leads to thin arms and legs) -Menstrual cycle disturbances |
| What other conditions are patients with cushing's syndrome at risk of? | -renal calculi -Predisposition to infection (also means wounds heal more slowly) -Hypertension -Predisposition to CCF -Osteoporosis, vertebral collapse -predisposition to glucose intolerance/diabetes |
| What tests are performed in a patient you suspect has excess prolactin? | -Baseline blood test (because prolactin levels remain fairly constant. Measured between 9am and 4pm -MRI imaging, most common cause of excess prolactin is a prolactinoma. Patient should be asked about dopamine antagonist use (eg clozapine) because these may cause menstrual distubancesand galactorrhoea as side effects. A thyroid function test should also be done since excess TRH (i.e in primary hypothyroidism when there is no negative feedback from thyroid hormones) can also stimulate prolactin release. |
| How is hyperprolactinaemia treated? | Usually treated by giving the patient a dopamine agonist. A prolactinoma is the most common cause but unline most other endocrine tumours, surgery is a second line treatment because giving a dopamine agonist usually has a profound effect in reducing the size of the tumour and improving symptoms. Surgery may be indiciated in extremely large tumours, especially if the patient's eyesight is threatened. Cabergoline or bromocriptine are the dopamine agonists often used. This is because the dopamine released from the hypothalamus has an inhibitory effect on prolactin release from the pituitary. |
| What are the causes of hypoerprolactinaemia? | Most common cause is a pituitary adenoma. other causes include disinhibition by reducing local dopamine levels eg from pituitary stalk compression. Also by administration of a dopamine antagonist eg metaclopramide. |
| What are the clinical symptoms of hyperprolactinaemia? | Female - decreased libido -Weight gain -amenorrhoea -galactorrhoea -Infertility Male - reduced facial hair -Impotence -galactorrhoea |
| What other conditions are patients who have hyperprolactinaemia at risk of? | male and female - osteoporosis -Neurological signs (from pressure of pituitary tumours |
| In hypopituitarism, which hormones are tested for in a basal blood test and which are done with dynamic testing? | Basal tests are done for -prolactin -TSH (and T4) -LH -FSH Dynamic tests are done for - GH (insulin tolerance test) -ACTH (insulin tolerance test or short synacthen test) |
| What are the causes of hypopituitarism? | 1) non functioning pituitary adenoma 2) other tumours in surrounding tumours compressing the pituitary gland 3) infarction of the pituitary eg sheehans 4) compression of the pitutiary gland eg empty sella 5) trauma 6) hypophysectomy or radiotherapy |
| Give the clinical symptoms and signs of a patient with corticotrophin deficiency | -dizziness -nausea -postural hypotension -breast atrophy -weight loss Patient may also have hyponatraemia |
| Give the clinical symptoms of a patient with thyroid hormone deficiency | -weight gain -dry skin -constipation -low mood |
| Give the clinical symptoms and signs of a patient with gonadotrophin deficiency | -oligomenorrhoea/amennorrhoea -decreased libido patients are often infertile and have osteoporosis |
| Give the clinical symptoms and signsof a patient with androgen deficiency | -hair loss -decreased libido -erectile dysfunction patient also has hypogonadism |
| Give the clinical symptoms of a patient with growth hormone deficiency | -truncal obesity -weakness patient may also have atherosclerosis, decreased cardiac output and osteroporosis |
| What is the name of the condition when a lack of ADH results in dilute urine and a constant thirst? | Diabetes insipidus |
| What is the first investigation are performed if you suspect a patient has a problem with their ADH release? | 1) water deprivation test - patient is deprived of food and water for a night then for 8 hours the following day. Plasma and urine osmolality is monitored regularly. the patient's weight is also monitored and the test is abandoned if more than 3% body weight is lost. If urine osmolality remains low then the patient can be diagnosed with diabetes insipidus. |
| If a patient has been confirmed as having diabetes insipidus, what is the second investigation carried out? | Desmopressin test - find out whether problem is lack of ADH (cranial DI) or insensitivity of the ADH receptors in the kidney (nephrogenic DI). Done immediately after the water deprivation test so that the patient is still fasted and dehydrated. Desmopressin, an ADH analogue is given and the patient is given water to drink. The urine and plasma osmolality is measured 2 hours later. If the problem is cranial DI, then giving an analogue should return the osmolalities to normal. If it is nephrogenic, then desmopressin will have no effect. |
| What are the symptoms of diabetes insipidus? | -Polyuria -dilute urine -polydipsia -dehydration |
| What are the causes of cranial DI? | -head injury -Hypophysectomy -metastases -Pituitary tumour -meningitis -vascular lesion -sarcoidosis -inherited -idiopathic (usually self limiting) |
| What are the causes of nephrogenic DI? | -Low potassium -High calcium -Drugs eg lithium -pyelonephritis -hydronephritis -inherited -pregnancy (rare as a primary cause |
| How is DI treated? | Cranial - life long treatment with desmopressin given intransally. Nephrogenic - correcting the cause and if symptoms continue, giving bendroflumethiazide. |
| What is the name given for excess ADH and what can this be a cause off? How can this cause be distinguished form the other causes of this condition? | SIADH cause of hyponatraemia. 1) patient is not dehydrated/no hypovolaemia 2) no oedema 3) concentrated urine 4) no diuretic used |
| What are the signs and symptoms of hyponatraemia? | symptoms - confusion -nausea -muscle weakness signs - hypertension -cardiac failure -low serum sodium |
| With regards to the breast, a hard, irregular, tethered lump is indicative of... | Breast carcinoma |
| With regards to the breast, a smooth, rounded and mobile lump is indicative of.... | A breast cyst or fibroadenoma |
| Diffuse nodularity of the breast suggests a.... | Fibrocystic change |
| What is the most common cause of nipple retraction in young women? | Duct ectasia |
| Which two views are taken in a mammography? | -Mediolateral oblique including the axillary tail - Craniocaudal |
| Describe the advantages and disadvantages of performing mammography | Advantages - ability to identify pre-malignant lesion eg DCIS -Able to pick up non-palpable lesions Disadvantages - uncomfortable - less reliable at detecting abnormalities in younger women due to the increased density of their breast tissue -Not suitable for screening large breasts -Exposure to ionising radiation -fails to detect at least 10% of breast cancers |
| Describe the advantages and disadvantages of performing ultrasound imaging of the breast | Advantages - no exposure to ionising radiation -easy to perform -relatively painless -sensitive at differentiation solid tumours from cysts Disadvantage - more operator dependent |
| What are the main differentials of a stellate mass on mammogram? | A stellate mass (appearance of lines radiating out from a central scar) on mammogram is normally either a radial scar (a benign, localised area of excessive fibrosis or sclerosis). Second differential is a carcinoma, needs to be sent for biopsy. |
| What surgical procedures are carried out in breast cancer? | Breast surgeries - wide local excision -Mastectomy Axillary surgeries - axillary block dissection -axillary node sampling (minimum of four nodes are located by palpation and excised for histological analysis - sentinel node biopsy - a radioisotope and/or blue dye which travel to the axillary lymph nodes is injected into the breast. The tracer is used to identify the sentinal node, which is the first node in the chain of lymph nodes and therefore most likely to contain a tumour which is then sent for histological analysis. |
| What are the pros and cons of axillary block dissection? | Pros - allows full histological assessment and effectively treats axillary metastatic spread Cons - 60-70% of patients don't have axillary metastases and the operation frequently leads to lymoedema of the arm and some numbness and paraesthesia |
| Which reconstructive surgeries are performed in women with breast cancer? | -breast implants -lattisimus dorsi flap -traverse rectus abdominal muscle (TRAM) flap -Deep inferior epigastric perforator (DIEP) flap |
| When is radiotherapy used in breast cancer? | Following WLE of a breast carcinoma (without, recurrence rates are 40%, with, rates are only 6%) Also used after mastectomy if tumour had risk factors for local recurrence |
| When is hormone manipulation therapy used in breast medicine? Give examples of agents used some extra info on them | -Used in cancers that are positive for oestrogen or progesterone receptors. Also used in advanced breast cancer. 1)Tamoxifen (oral anti oestrogen) 2) Aromatase inhibitors (anastrozole, exemestane, letrozole. Prevents conversion of androgens to oestrogens. 3) Goserelin (LHRH agonist) Tamoxifen carries risk of thromboembolic episodes (pre-menopausal women). Anastrozole better than tamoxifen at preventing disease relapse (post menopausal women) |
| When is chemotheapy used in breast medicine, give some example of agents and info on them. | -in addition to hormone manipulation therapy for hormone receptor positive disease. Also for hormone receptor negative tumours. -Combination of drugs always used eg 5-FU, epirubicin, cyclophosphamide -Adjuvant chemotheapy is far more effective in young women. -Little benefit and increased side effects in older women |
| When is immunotherapy used in breast medicine, give some examples of agents and some extra info on them. | -patients testing positive for HER2 overexpression. -Trastuzumab (herceptin) -Prolongs survival in women with advanced disease -given IV -Cardiotoxic |
| What are the four main pathological processes involved in a fibrocystic breast change? | -Adenosis -Epitheliosis -Fibrosis -Cyst formation |
| describe the aetiology of acute bacterial mastitis | Normally second to staphylococcus aureus infection of the breast which usually gains entry to the breast through cracked nipples. |
| Describe the differences in pathology between acute bacterial mastitis and periductal mastitis | Acute bacterial - infecting process lactational = usually S. aureus Non-lactational = common organisms include alpha haemolytic streptococci, enterococci and bacteroides. Periductal mastitis - inflammatory process occurring around dilated milk ducts near the nipple. |
| Describe the differences in age range between acute bacterial mastitis and periductal mastitis | acute bacterial - 20-40 years old Periductal - premenopausal women |
| Describe the differences in history/examination between acute bacterial mastitis and periductal mastitis | acute bacterial - acute, painful, hot, red swelling adjacent to the nipple within first 6 weeks of breastfeeding. -No nipple discharge -may be a history of a cracked nipple Periductal - may present with: - nipple discharge -Tenderness -Chronic painful swelling with cellulitis -Nipple retraction -Mass deep to nipple -Fistula formation Link to smoking and nipple piercings increase likelihood of infection. |
| Describe duct ectasia | -involutional change in the ducts assocaited with the menopause -Terminal ducts behind the nipple become dilated (ectasia) and engorged with secretions -Chronic process -Nipple discharge and/or nipple retraction (characteristic appearance of a transverse, slit-like nipple, frequently bilateral) -Cytological analysis of the fluid shows macrophages and chronic inflammatory debris. Secondary infection can lead to a retroareolar abscess. |
| How is the anterior triangle of the neck further divided and what are the contents of each triangle? | Submental triangle - Superiorly = chin, Laterally = two anterior bellies of digastric, Medially = the midline. Contents = submental lymph nodes Submandibular triangle -boundaries are the bellies of the digastric muscles and the mandible. Contains the submandibular salivary glands and lymph nodes Carotid triangle - superiorly= posterior belly of digastric, laterally = anterior border of SCM, medially= superior belly of omohyoid. Contains the carotid artery, the IJV, vagus nerve and internal and external laryngeal nerves. Muscular triangle - boundaries are the superior belly of the omohyoid muscle and the sternohyoid muscle. Contains the deep structures including the larynx, trachea, thyroid and the oesophagus |
| How is the posterior triangle of the neck further divided and what are the contents of each triangle? | occipital triangle (larger subdivision) - anteriorly = SCM, posteriorly = trapezius, inferiorly = omohyoid. Supraclavicular triangle - anteriorly = posterior border of SCM, superiorly = inferior belly of omohyoid, inferiorly = clavicle. Mostly lumps arising from the posterior triangle are due to enlarged occipital or supraclavicular lymph nodes. Other important structures include the subclavian artery, EJV, accessory nerve, phrenic nerve and parts of the brachial plexus. |
| What mnemonic can be used for describing a neck mass? | 4 S's 3 C's 3 T's -Site, size, shape, surface -Consistency, colour, compressible/fluctuant -transillumination, tenderness, tethered |
| Give some causes of lymphadenopathy | Infective - viral (infectious mononucleosis, HIV). Bacterial (any bacterial infection of the head/neck, TB) Malignant - Lymphoma or mets |
| Firm rubbery non-tender lymph nodes are usually associated with.... | Lymphoma |
| Where do tumours from the head and neck normally metastaise to | Nodes in the submandibular region and the upper part of the anterior triangle. |
| Where do tumours of the chest and abdomen usually metastaise to in the necl? | Lower part of the posterior triangle. |
| Where does a branchial cyst present and how do they arise? | Presents as a smooth swelling in front of the anterior border of SCM at the function of the upper and middle thirds. Branchial cysts arise from the embryonic remnant of the second branchial cleft in the neck. They most commonly occur in young adults. They may enlarge during a URTI then persist. The lump itself is soft and fluctuant and may transilluminate. |
| Describe a laryngocele | Painless lesion found in the anterior triangle. Dilatation of the laryngeal saccule above the superior margin of the thyroid cartilage. Narrow blind ended pouches which communicate with the laryngeal lumen and may bulge outward on the neck. They contain air or become distended with mucous. May be internal (confined to the larynx) or mixed (herniates through the thyrohyoid membrane and has both internal and external components). They can be congenital or acquired due to continual forced expiration producing increased pressures in the larynx. Seen in glassblowers, players of wind instruments and people with chronic obstructive airway disease. |
| What are cervical ribs and why are they a problem? | Rare congenital abnormality that lies above the first rib. Arises from the 7th cervical vertebra. Associated with thoracic outlet syndrome due to compression of the lower trunk of the brachial plexus or subclavian artery. |
| Describe a carotid body tumour | Found in the posterior triangle of the neck. Arises from the chemoreceptor cells in the carotid body and are classically located in the carotid bifurcation, between the internal and external carotid arteries. They typically present as painless neck masses just lateral to the tip of the hyoid bone, the mass transits a carotid pulsation. Slow growing and most behave in a benign fashion. Pressure on the carotid sinus from the tumour can cause attacks of faintness and growth of the tumour may lead to cranial nerve palsies. |
| What are cystic hygromas? | Single or multiple cysts classically found inthe left posterior triangle of the neck. Benign lesions comprised of lymph filled sacs that originate from an embryonic remnant of the jugular lymph sac. May present at brith as a congenital defect, which can be large and disfiguiring. May also develop in older children presenting as a smaller painless lump below the angle of the mandible. Cystic hygromas are soft, fluctuant and transilluminable. |
| What is the most likely diagnosis of a neck lump in the anterior triangle, presenting as a smooth swelling in front of the anterior border of the sternocleidomastoid muscle? | Branchial cyst |
| What is the most likely diagnosis of a neck lump in the anterior triangle, presenting as a painless, smooth, cystic, midline swelling that moves upward on swallowing and on protrusion of the tongue? | Thyroglossal cyst |
| Which disease of the neck is palmar erythema a sign of? | Thyrotoxicosis |
| What is onycholysis and what is it a sign of? | Where the nail separates itself from the nail bed. Can be seen in thyrotoxicosis |
| What is thyroid acropachy? | Due to subperiosteal bone formation and usually presents as finger clubbing. It is only seen in graves disease and is a rare finding. |
| What is facial myxoedema and in which condition is it seen? | Puffiness of the face and can be seen in hypothyroidism. Loss of the outer third of the eyebrow might also be observed on examination. |
| What are exophthalmos and lid retrtaction signs of and how do they occur? | Exophthalmos can be seen in hyperthyroidism and is due to swelling of the extraocular eye muscle. On clinical examination, the eyes appear to protrude from the eye socket and the sclera becomes visible below the lower limbus of the iris. Lid retraction can be seen in hyperthyroidism. It occur due to increased stimulation of the sympathetic nerves to the eye lids. This causes the eyes to remain wide open resulting in the sclera becoming visible above the upper limbus of the iris. |
| infront of which tracheal rings does the thyroid gland lie? | Second to fourth |
| What is the classical triad of graves disease? How is this disease caused? | exophthalmos, goitre and pretibial myxoedema Autoantibodies are produced against TSH receptors, and the IgG antibodies behave like TSH and bind the receptor on the thyroid cell, stimulating them to produce thyroid hormones in excess and the thyroid gland to grow. |
| What is the most common cause of hypothyroidism? | Iodine deficiency. In non-iodine deficient areas, hashimoto's thyroiditis. Autoimmune disease, typically there is aggressive destruction of the thyroid cell by various immune processes, causing the gradual destruction of the gland itself. |
| What is De Quervain's thyroiditis? Describe the pathogenesis and how it is treated. | Cause of hypothyroidism. Inflammation of the thyroid gland caused by viral infection. Rare but more common in young or middle aged women. Usually presents as a tender, swollen, firm gland often following a viral URTI. Initial inflammation causes an increase in TH release, causing transient hyperthyroidism. It is often self limiting and at this stage and treatment includes NSAIDs (or steroids) and beta blockers for symptomatic control. However, this initial inflammatory stage may be followed by destruction of the follicles, which leads to hypothyroidism and leakage of the thyroglobulin colloid. Immune reaction to thyroglobulin causes the formation of granulomas, hence why the condition is known as granulomatous thyroiditis. may need to be treated with exogenous thyroid hormone, or may self resolve. |
| What are patients who are on antithyroid drugs at risk of? How should this be managed clinically? | Bone marrow suppresio.nAntithyroid drugs such as carbimazole and propylthiouracil can cause neutropaenia and agranulocytosis. You should advise patients starting antithyroid drugs that if they experience sore throats, mouth ulcers, unexplained bruising or bleeding, rash, fever or any other indications of infection to stop drug immediately and see doctor for a FBC. |
| Describe the genetics of medullary thyroid carcinomas | Approximately 25% are familial, caused by a mutation in the RET proto-oncogene. |
| Where do the four types of thyroid tumours metastasise to? | Papillary and medullary - cervical lymph nodes Follicular - invade blood vessels and metastasise to bone, lungs and brain. Anaplastic invades locally. |
| What is fatiguable weakness of muscle groups associated with? | Problems at the NMJ. Think MG |
| Describe the muscles that are used in the hand to test the integrity of the three nerves of the hand | Abductor pollucis brevis - median nerve First dorsal interosseous - ulnar nerve Finger/wrist extenors - radial nerve |
| Where does the olfactory nerve enter the brain stem? | It doesn't, the olfactory and the optic nerve enter the cerebral cortex directly. |
| What makes the olfactory pathway unique? | It is entirely ipsilateral |
| Would a patient with an olfactory nerve lesion be able to smell ammonia? | Yes - patients still able to sense a noxious gas. Ammonia can be used in the clinical assessment of the olfactory system because it is in fact detected by the nasal epithelium which is innervated by the trigeminal nerve |
| Describe the general rule of thumb for abdominal pain and where it refers to | 1) Deep, poorly localised pain in the midline = visceral abdominal pain from distension of hollow organs (sympathetic splanchnic nerves) think unpaired structures eg ileum 2) Lateral pain localised to area of inflammation = somatic pain from parietal peritoneum and abdominal wall (intercostal spinal nerves) think paired structures eg kidneys 3) organs of the foregut cause pain in epigastic 4) organs of midgut cause pain i periumbilical region 5) organs of hindgut caused pain in hypogastric region Peritoneal inflammation next to the diaphragm causes referred pain to the shoulder tip |
| What are the red flags in patients with abdominal pain? | -Leaking bowel contents from a perforated ulcer causes generalised peritonitis. Look out for sudden onset severe epigastric pain, which rapidly becomes generalised and constant -Associated breathlessness, palpitation or other CVS disease suggests a vascular event like a ruptured aortic aneurysm or mesenteric ischaemia. -A female with a missed period and sudden onset lower abdominal pain with discharge may have an ectopic pregnancy -Upper abdominal pain, nausea, vomiting and anorexia with fluid imbalance (hypovolaemia, shock or peripheral oedema) suggests acute pancreatitis |
| What does sudden onset severe abdominal pain suggest? | Likely to either be a vascular event eg ruptured AAA or ischaemia bowel... or a perforated viscus eg ulcer, appendix or diverticulum. Pain from inflammation or infection is slowly progressive |
| Describe biliary colic | Constant pain, rapidly increasing to peak intensity and then gradually resolving over several hours. the patient will be restless and unable to lie still |
| What things are suggestive of an upper GI BLEED? | Haematemesis and malaena suggest an upper GI bleed, whereas fresh red blood suggest a lower GI pathology. |
| How is a blood test used to diagnose pancreatitis? | Serum amylase elevated to 5x normal levels in the first 5 days after symptoms begin is diagnostic for pancreatitis. (normal levels 40-140) |
| What are the three most useful diagnostic bedside tests for local peritonitis? | 1) Blumberg's test - blumbergs sign (rebound tenderness) indicates local peritonitis Cough test - this rapid change in abdominal pressure moves the irritated peritoneal lining, causing pain Hip flexion test - flexing the hip on the affects side stretches the irritated peritoneal lining, causing localised pain that suggests peritonitis. |
| Give five causes of generalised peritonitis | 1) chemical irritation from perforated peptic or duodenal ulcer 2) leaking bile from ccholecystitis 3) infection from ruptured appendix 4) faecal matter from diverticulitis 5) deterioration of local peritonitis from inflammatory condition |
| What is the clinical presentation of generalised peritonitis | -Severe abdominal pain, worse on movement -Patient lies very still -Tender abdomen with eashboard rigidity, rebound tenderness, guarding, and absent bowel sounds -Hypovolaemic shock may occur |
| What investigations are used to diagnose generalised peritonitis? | -CT abdo (to determine cause) -Serum amylase (to rule out pancreatitis) |
| What is the management for generalised peritonitis? | 1) resuscitate with IV fluids with careful fluid balance monitoring until a good urinary output is maintained (NG tube, urinary catheter, IV fluids) 2) infuse IV antibiotics 3) prompt laparotomy/laparoscopy (peritoneal wash-out, and treatment of the underlying condition) 4) monitor for development of post-operative complications |
| What are the complications of peritonitis if not treated? | Can rapidly deteriorate with further toxaemia, septicaemia and multi organ failure |
| What are the risk factors for peptic/duodenal ulcers? | -NSAID use -Alcohol -Smoking -H. pylori -Steroids -Blood group O |
| How can peptic ulcers become life threatening? | 1) they can either erode blood vessels causing upper GI bleeds which present with haematemesis and/or meleana. These patient may have epigastric discomfort, but they do not present with acute abdominal pain 2) Can erode through the mucosa to cause a bowel perforation. Gastric or duodenal contents leaks into the peritoneum, causing an acute generalised peritonitis. |
| What mnemonic is used to predict perforation risk for a peptic/duodenal ulcer? | ALARMS A - Anaemia L - loss of weight A - anorexia R - recent onset or progressive symptoms M - meleana or haematemesis S - swallowing difficulty |
| What is the classical presentation of a perforated gastric or duodenal ulcer? | -Patient with a history of meal related dyspepsia -sudden acute onset abdominal pain -often followed by collapse and shock -generalised peritonitis on examination of the abdomen -Pneumoperitoneum on erect CXR -H. pylori positive at breast test |
| What is the treatment of H. pylori positive on breath test? | Triply therapy including a PPI, amoxicillin and clarithromycin. |
| What are the complication of pancreatitis? | Inflammation of pancreatic and retroperitoneal tissue causes fluid shifts, which can rapidly deteriorate from mild oedema to hypovolaemia, ascites and extensive peripheral oedema |
| What are grey-turner's a nd cullen's signs and why are they important? | Autodigestion by pancreatic enzymes in pancreatitis causes necrotising and/or haemorrhagic pancreatitis. these clinical signs develop from bruising into the falciform ligament, blood vessel autodigestion and retroperitoneal haemorrhage. |
| Which pneumonic helps to remember the causes of pancreatitis? | I GET SMASHED I - idiopathic G - gallstones E - ethanol T- trauma S - steroids M - mumps A - autoimmune S - scorpion venom H - hyperlipidaemia, hypothermia, hypercalcaemia, E - ERCP and emboli D - drugs |
| How is pain from pancreatitis relieved? | By sitting forward |
| What are the complications of severe pancreatitis? | -Diabetes due to autodigestion of beta cells in islets of langerhans -Renal failure from hypovolaemia -peritonitis develops as infection spreads throughout the peritoneal cavity -Abscess or fistula formation -haemorrhage -thrombosis -shock |
| What investigations are used to diagnose pacreatitis? | -Serum amylase - >1000 u/ml in many Gi conitions (including pancreatitis) and is inaccurate if renal failure co-exists -Serum lipase - is more sensitive and specific for a diagnosis of pancreatitis -CPR and ESR - to assess inflammatory markers -ABG - to monitor oxygenation and acid-base levels -AXR - loss of psoas shadow indicates shift of fluid to retroperitoneum -Erect CXR - to rule out perforated viscus as a cause -CT scan - assess severity of inflammation/necrosis -Ultrasound - if suspected cause is gallstones |
| What is the management of acute pancreatitis? | Drip and Suck Patients should be nil by mouth to allow for complete bowel rest -The drip refers to IV therapy - fluids and analgesia, and insert a urinary catheter to monitor fluid balance (aim for urinary output >30ml/hr) -The suck refers to an NG tube - insert a wide bore NG tube (ryle's tube) to drain gastric contents. This also ensures the bowel is rested and can help with symptoms or nausea and vomiting through relief of gastric distension. |
| What is the most important investigation in a patient presenting with what you believe is generalised peritonitis? | Check serum amylase - if raised, pancreatitis |
| What are gall stones? | Calcification of cholesterol and bile pigments |
| What is cholecystitis? | Inflammation of the cystic duct and gall bladder caused by a gall stone obstruction. LFTs may be elevated, CRP and WBCs high. Untreated cholecystitis can lead to cholangitis |
| What is cholangitis? | Inflammation of the common bile duct. Presents very similarly to cholecystitis and is managed the same; however blood tests will show an elevated bilirubin, Alkaline phosphatase and gammaGT (like obstructive jaundice). Untreated cholangitis can lead to ascending cholangitis. |
| What is ascending cholangitis? | Infection in the common bile duct (usually bacterial) spreads to encompass the entire biliary tree, including the hepatic ducts in the liver. The triad of symptoms are abdominal pain in the RUQ, jaundice and fever. Patients may also have septic shock and acute confusion. |
| What is the clinical presentation of acute cholecystitis? | -initial biliary colic -Leading to sever RUQ pain, fever, nausea, vomiting and anorexia -Tenderness and guarding in the RUQ on examination -Referred pain from an irritated diaphragm may cause pain in the shoulder tip -Murphy's sign positive -Obstructive jaundice and cholangitis may develop if the stone dislodges and settle in the common bile duct. |
| What are the investigation for cholecystitis? | -blood tests will show elevated WCC and CRp -LFTs will be normal unless CBD obstruction or cholangitis develop -Ultrasound - |
| What is the management of cholecysitits? | -Nil by mouth -IV fluids, and opiate analgesia -IV anitibiotics eg cefuroxime -Urgent cholecystectomy if fever worse, pain intensifies or if gangrene or empyema develop -Otherwise elective laparoscopic cholecystectomy when symptoms settle |
| Elevated Alk. phos and bilirubin, pruritis and icterus. What is this complication of gall stones? | Obstructive jaundice |
| Jaundice, RUQ pain, rigors, elevated CRP. What is this complication of gall stones? | Ascending cholangitis |
| Epigastric pain, anorexia, vomiting, oedema. What is this complication of gall stones? | Acute pancreatitis |
| Distended abdomen, generalised tenderness, absent bowel sounds. What is this complication of gall stones? | generalised peritonitis. |
| What is the appendix? | Worm like protrusion of the caecum, hence it is known as the vermiform appendix. Whilst it is generally agreed that it no longer has a function, the appendix is believed to have housed bacteria that aided primates in digestion of cellulose when eating plants. |
| What is the pathophysiology of appendicitis? | Believed to be caused by obstruction of the appendiceal lumen. Luminal secretion continues while it is obstructed and the stagnant secretions allow bacteria in the lumen to multiply. This leads to inflammatory response in the appendix. The cause of obstruction is either 1) lymphoid hyperplasia - the appendix contains several lymphoid follicles which can inappropriately multiply in inflammatory and infectious conditions such as Crohn's, amoebiasis, respiratory infection, mononucleosis and measles. 2) Infection - common in children and young adults 3) fecal stasis and fecaliths - fecaliths are compacted lumps of faeces and calcium salts (common in elderly) 4) Less commonly - bacteria, parasites, foreign bodies, TB and tumours. |
| What are the peak ages for appendicitis? | 10-19 years |
| When are instances of appendicitis more common? | More frequently during the summer. Reasons unclear but may be related to seasonal variation of viral infections. |
| What is the clinical presentation of acute appendicitis? | 1) pain - periumbilical and anorexia followed by nausea and R iliac fossa pain (50% of cases). Pain migration from umbilicus to Mcburney's point has an approximately 80% sensitivity and specificity. 2) abdo symptoms - nausea present (61-92%) and anorexia (74-78%). Important to note progression and timing of symptoms. 3) others - Inflamed appendix near the bladder or ureter can cause painful voiding and haematuria or pyuria. |
| What are the signs of appendicitis? | 1) Psoas sign - if the appendix is located behind the caecum, it will lie close to the iliopsoas muscles, the hip flexors. To elicit the sign ask the patient to raise their leg against resistance. If increased pain is experienced in the right iliac fossa, this is a positive psoas sign. it can also be elicited by asking the patient to roll onto their left side and extent their right leg. 2) obturator sign - internal obturator muscle lies close to the appendix. To elicit the sign bend the patients right knee and flex their hip, then internally rotate the hip. This stretches the internal obturator, increased pain in the right iliac fossa is a positive sign. 3) Rovsing's sign - sign of appendiceal inflammation. Press deeply and slowly in the left iliac fossa and remove your hand quickly. Rosving's sign is positive if increased pain is felt in the right iliac fossa. |
| What is the accuracy rate for the diagnosis of acute appendicitis? Which demographics are most commonly misdiagnosed? | 80%. 1) women of child bearing age - rate of misdiagnosis is 33%. Misdiagnoses commonly include pelvic inflammatory disease, urinary tract infections and gastroenteritis. 2) Children - misdiagnosis rate of 25-30%. They are commonly misdiagnosed with gastroenteritis followed by upper and lower RTIs. 3) Misdiagnosis is higher in the elderly. tend to present later. |
| How can examination and investigations steer yours diagnosis of appendicits in women of child bearing age? | On examination, tenderness outside the lower right quadrant, cervical motion tenderness, vaginal discharge and positive urinalysis support PID. The level of beta-HCG can help differentiate between appendicitis and an ectopic pregnancy. Have a high rate of suspicion for appendicitis in pregnant women as perforation can be fatal for the fetus. |
| A 25 year old woman presents to the emergency department with a 24 hour history of right lower quadrant pain, nausea and anorexia. What is the most likely diagnosis? What would be found on investigation in this patient? | Appencitis. Raised CRP and WCC. |
| A 45 year old man presents to his GP with intermittent upper abdominal pain that does not radiate anywhere and is worse on lying down and after eating. The surgery has no records of his vaccinations. What is the most likely diagnosis? | GORD |
| A 19 year old woman presents to the emergency department with lower abdominal pain, fever and dysuria. She admits to recently having unprotected sex. Urinalysis is negative for protein or leukocytes. What is the most likely diagnosis? | PID |
| A 35 year old male presents to the emergency department with lower right quadrant pain, constipation, vomiting. He has a history of gallstones and thinks he had his gallbladder removed. FBC, CRP and U and Es have come back normal. What is the most likely diagnosis? | Intestinal obstruction |
| What is the alvarado score used for, describe it. | For acute appendicitis management Migration of pain (1), anorexia (1), Nausea (1), tenderness in RIF (2), rebound tenderness (1), elevated temperature (1), leukocytosis (2), Shift of WBC to left (increase in ratio of immature WBCs to mature WBCs). Score 1-4 = discharge/watchful waiting 5-6 = observation/ admission. 7-10 = surgery |
| Give examples of bowel obstruction | Can either be mechanical or non-functioning. Mechanical - hernias, adhesion from previous abdominal surgery, constipation, diverticulitis, gall stones, crohn's disease, intussusception, volvulus, tumour, foreign object Non functioning - paralytic ileus, generalised peritonitis and after GI tract operations. |
| What are the symptoms and signs of bowel obstruction? | Symptoms - sudden onset colicky central abdominal pain - Vomiting (more profuse in small bowel obstruction) -Absolute constipation (not even passing wind) -Nausea, anorexia -Abdominal distension Signs - Distension (progressive) -palpable mass, or visible surgical scars, or hernia -Visible peristalsis -Absent or tinkling bowel sound -If there is marked tenderness beware of bowel strangulation, a surgical emergency. prompt surgery is required to prevent ischaemic damage. |
| How do you distinguish between small and large bowel obstruction? | Small bowel obstruction produces less distension, earlier vomiting and pain higher in the abdomen than large bowel obstruction. |
| How do you distinguish betwee large and small bowel obstruction of plain X ray? | -Small bowel obstruction has no distal gas and distended bowel would have valvulae conniventes (transverse lines across the bowel that are unbroken) rather than haustra of the large bowel. |
| What is the management of bowel obstruction? | Similar to drip and suck 1) IV fluids to rehydrate and correct any electrolyte imbalances caused by vomiting 2) insert wide bore NG tube (ryle's tube) to relieve gastric distension 3) don't forget IV analgesia and urinary catheter to monitor fluid balance 4) test serum blood for amylase, FBC and U&E to rule out other causes 5) CT abdo to identify location and cause of obstruction, and decide whether surgery is required 6) Some large bowel obstructions can be relieved by flexible sigmoidoscopy to unkink the colon; however there is a risk of causing further damage including a perforation. |
| Describe how diverticula form | -Diverticula form when high intraluminal pressure causes a pouch of mucosa to extrude through the weakened muscular wall of the large colon. Diverticula are common and associated with ageing. it is thought the pressure of hard stools passing through the intestine that has become weakened with age causes bulges to form. they are more common in western population who have low fibre diets. |
| how common are diverticulas? | Estimates suggest that half the population have diverticula by the time they are 50 and 70% have them by the time they are 80. |
| Define diverticulosis | Refers to the presence of diverticulae, which is either uncomplicated or causes simple constipation, bloating, cramping or flatulence. Most people with diverticulae will complain of symptoms such as this. |
| Define acute diverticulitis. What is the clinical presentation? | Develops when stagnant faeces causes bacterial accumulation of infection within a diverticula. Patients present with acute LIF pain, fever, tachycardia and localised peritonitis. There may be a palpable mass if a diverticula abscess has developed as a complication. |
| What is the treatment of acute diverticulitis? | IV fluids, analesia and Abx. laxatives and increased dietary fibre are important in prevention. Surgery can be needed in complicated or severe cases. Sigmoidoscopy is useful in diagnosis of diverticular disease, but should not be attempted during an acute diverticulitis due to increased risk of perforation. |
| How can diverticuliis lead to tachycardia, hypotension, pallor, thirst and hypothermia? | Diverticulae form at sites of blood vessel supply, and when the inflammation invades blood vessel walls haemorrhage into the abdominal cavity can follow, resulting in hypovolaemic shock. |
| How can diverticulitis lead to dysuria, vaginal discomfort and cystitis? | Fistulae can form to either the bladder or vagina causing a UTI or vaginal infection from bowel contents. |
| Give a brief clinical summary of diverticulitis | Diverticulitis is infected diverticulosis, causing acute abdominal pain in the iliac fossa. Treat with antibiotics and analgesia, whilst monitoring for further complications. |
| Give a brief clinical summary of perionitis | Generalised peritonitis presents with generalised pain & tenderness, a rigid, distended abdomen, and absent bowel sounds. Urgent resuscitation, ABX and peritoneal wash-out are required. |
| Give a brief clinical summary ofperforated ulcers | Perforated ulcers leak acidic gastric contents into the peritoneum, and require urgent surgery to both repair the damaged mucosae, and wash out the peritoneal cavity. Look for ALARM Symptoms in any patient with meal-related dyspepsia. |
| Give a brief clinical summary of pancreatitis | Acute pancreatitis can be life-threatening. Urgent fluid resuscitation is essential as marked fluid shifts occur. Management is supportive via a 'drip and suck' regime. Pancreatitis can mimic generalised peritonitis, so always check serum amylase. And remember, antibiotics don't help! |
| Give a brief clinical summary of cholecytisi and gall stone disease | Gall stone disease is often benign, but can lead to cholecystitis and acute pancreatitis (presenting with an acute abdomen), ascending cholangitis, obstructive jaundice, empyema, and abscess formation, leading to peritonitis. |
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