Year 3 revision - chapter 2 Flashcards
1
Q
What are the features of diverticular bleeding?
A
A diverticular bleed is abrupt and of significant volume, but settles in 80% of cases.
2
Q
What antibiotics would you use for diverticulitis?
A
NotesRecent trials have suggested that antibiotic therapy may not be required for patients with mild abdominal pain and tenderness who do not have significant systemic signs or symptoms.Antibiotics should be considered in patients with signs of diverticulitis who have markers of systemic involvement (eg fever, elevated white cell count), or in patients who have failed to respond to conservative management.Remember that Tazocin and Timentin cover G+, G-, enterococci and anaerobes
3
Q
How common are diverticula?
A
50% of people over age 50
4
Q
What symptoms would make you worry/further investigate a patient with diagnosed irritable bowel syndrome?
A
Pain associated with anorexia, malnutrition, or weight loss.Pain that is progressive, awakens the patient from sleep, or prevents sleep.
5
Q
What is the difference between a gastric erosion and a gastric ulcer?
A
PUD is classified as a break in the mucosal lining of the stomach or duodenum > 5mm in depth* involving the SUBMUCOSA.(* note that erosions differ from ulcers in that they are
6
Q
What are the 2 most important causes of peptic ulcer disease?
A
Helicobactor pylori infectionNon-steroidal Antiinflammatory drugs (NSAIDs)
7
Q
What are the features of pain caused by gastric/duodenal ulcers?
A
Chronic/recurrent abdominal pain or discomfort around epigastriumDuodenal ulcers: abdominal pain may be severe and radiate to the back as a result of penetration of the ulcer posteriorly into the pancreas..The “classic” pain of duodenal ulcers (DU) occurs when acid is secreted in the absence of a food buffer. Food is usually well emptied by two to three hours after meals, but food-stimulated acid secretion persists for three to five hours; thus, classic DU symptoms occur two to five hours after meals. Symptoms also classically occur at night, between about 11 PM and 2 AM, when the circadian stimulation of acid secretion is maximal.Painwhich is worse between meals or in the middle of the night, and eased by eating (= duodenal ulcer)Pain which is aggravated by eating (= gastric ulcer)
8
Q
What investigations are appropriate for peptic ulcer disease?
A
FBELook for anaemiaEndoscopy (+/- Biopsy)Do if ‘red flag’ symptoms –>upper GI cancerWeight loss/bleeding/anaemia/vomiting/early satiety/dysphagiaBiopsy the edge of the ulcer to DDx between simple ulcer and gastric adenocarcinomaH pylori testingIn the absence of ‘red flag symptoms’H pylori breath/stool antigen testsH Pylori serologyTests may give FALSE NEGATIVE results in patients taking PPI’s, bismuth or other medications.Switch to H2 antagonists before test
9
Q
What is Zollinger-Ellison syndrome?
A
A rare disorder caused by a gastrin-secreting tumor found in either the islet cells of the pancreas or in the duodenal wall. The release of gastrin stimulates the production of large quantities of HCL in the gastric antrum leading to predominant distal (duodenum) ulceration.
10
Q
What are the causes of haematemesis?
A
Very common * gastric ulcer/erosion * duodenal ulcer/erosion Common: * Mallory Weiss tear * ulcerative oesophagitis * oesophageal varices -->emergency Uncommon : * AVM (arteriovenous malformations) * Cancer * GIST * Aorto-enteric fistula
11
Q
What is the epidemiological relationship between cirrhosis, varices and death?
A
30% of cirrhotics have varices30% of varices haemorrhageVariceal haemorrhage has up to 30% mortality (depends on severity of liver disease)
12
Q
What are the causes of haematochezia?
A
Under 40 years Common * Haemorrohoids * Anal fissure * IBD Less common * Polyps * Infective colitis * Meckels diverticulum * Intussusception Rare * Colorectal cancer Over 40 years age * Haemorrhoids * Anal fissures * Colorectal cancer * Colorectal polyps (mostly adenomatous) * Angiodysplasia * Diverticular disease * Inflammatory bowel disease * Colitis – ischaemic, infective, post-radiation
13
Q
What are the causes of acute hepatitis?
A
Bacterial * Q fever * Typhoid * Syphilis Viral * Hepatitis A, B, C * Cytomegalovirus (CMV) * EBV * HSV Autoimmune * SLE * Autoimmune hepatitis Drugs (include but not limited to) * Amoxicillin-Calvulanic Acid (Augmentin) * Paracetemol (AST often rises above 5000) * Anti-Tuberculosis medications * Trimethoprim-sulfamethoxazole (Bactrim) * Minocycline * Nitrofurantoin
14
Q
Who does auto-immune hepatitis usually affect?
A
females in second and third decade of life
15
Q
What is the clinical picture of autoimmune hepatitis?
A
Onset may be insidious or acute. Can be anywhere from asymptomatic to fulminant hepatic failure.Symptoms are non-specific but may include:
* Fatigue/Malaise
* Nausea / Anorexia
* Abdo pain
* Jaundice/pruritis
* Signs of chronic liver disease, especially spider naevi and hepatospenomegaly
* Amenorrhea
* Rheumatological or thyroid complaints
Exam findings can range from a normal to the presence of hepatomegaly, splenomegaly, stigmata of chronic liver disease, and/or deep jaundice (rare).At the far end of the spectrum are those patients who present with an acute, sometimes fulminant picture characterized by profound jaundice, an elevated prothrombin time, and aminotransferase values in the thousands.
16
Q
What antibodies are associated with type 1 and type 2 autoimmune hepatitis?
A
Type 1 * antinuclear antibodies (ANA) * anti-smooth muscle antibodies (ASMA) Type 2 * anti-liver-kidney microsome-1 antibodies (ALKM-1) and * anti-liver cytosol antibody-1 (ALC-1)
17
Q
What is the management and prognosis of autoimmune hepatitis?
A
Management
* Patients have 45% chance of progression to cirrhosis
* The benefit of corticosteroids in asymptomatic patients with only histologic features is not clear (relatively few studies have elucidated the natural history of AIH in such patients) If decide to treat
* High-dose prednisolone (30-50mg/day for 6 weeks then titrate down)
* Add azathioprine as a steroid sparing agent to reduce AEs of steroids
* As a general rule, treatment should be continued until remission, treatment failure, or the development of drug toxicity
* Following steroid withdrawal, 75% of patients relapse.
Prognosis
* Can be severe: 40% mortality at 6 months without treatment.
* Appropriate management can improve quality of life, prolong survival, and delay the need for liver transplantation.
* The life-expectancy of treated patients is similar to age- and gender-matched controls in patients who have been followed for up to 20 years
18
Q
How contagious is Hep A?Who becomes symptomatic?
A
Highly infectiousFaecal-oral routeMost infections in adults are symptomatic, whereas 70% of infections in children younger than 6 years, who are also the key reservoir for transmission, are asymptomatic
19
Q
What test do you use for Hep A?
A
Anti HAV IgM and IgG (positive for 5-10days before symptoms)
20
Q
What is the management and prognosis of Hep A?
A
ManagementUnvaccinated people with recent exposure to hepatitis A (Symptomatic patients = Supportive care + bed restRarely, hospitalisation may become necessary for volume depletion, coagulopathy, encephalopathy, or severe prostration. This is particularly important in patients with co-infection with hepatitis B virus, hepatitis C virus, or cirrhosis of any cause, as acute hepatitis A virus (HAV) infection in these conditions has a higher risk for severe disease.In Prompt referral to centres experienced in liver transplantation is warranted in such cases.Prognosis≈85% have full clinical and biochemical recovery within 3-monthsnearly all individuals recover within 6 months10% to 20% of symptomatic patients –>prolonged and relapsing course lasting several months with persistent fever, pruritus, diarrhoea, jaundice, weight loss, and malabsorptionReported case fatality is 0.6% - 1.5% depending on age.
21
Q
How is Hep B transmitted?
A
Body fluidsNeedlstick/sharing needlesSTI (semen)Mother to baby
22
Q
What is the natural history of Hep B?
A
Most healthy adults (90%) who are infected will recover and develop antibodies against future hepatitis B infections. 5-10% will be unable to get rid of the virus and will develop chronic infections.This is not true for infants and young children – 90% of infants and up to 50% of young children infected with hepatitis B will develop chronic infections. Therefore, vaccination is essential to protect infants and children.Approximately 70% of patients with acute HBV infection are asymptomatic.About 30% of adults with acute HBV may have symptomatic icteric hepatitis.Patients who develop chronic HBV have a 10% to 30% risk of developing cirrhosis
23
Q
What tests constitute Hep B serology and how do you interpret them?
A
24
Q
What is the management of Hep B infection?
A
Acute = supportive careChronic
- Treatment is recommended in patients who are HBeAg-positive, with HBV DNA levels >20,000(IU)/mL
- Give pegylated interferon or antiviral monotherapy (tenofovir)
- The endpoint of treatment is seroconversion from HBeAg positive to HBeAg negative, with production of HBeAb.
25
How is Hep C spread?
Transmission is blood born only (very low risk of transmission from sexual activity.) In rare occasions can spread from mother to baby.
26
What is the natural history of Hep C?
27
What tests can you order for Hep C?
Anti-HCV antibodies(However this doesnt tell you if you're in the lucky 15% who cleared the infection)Active infection is confirmed by the presence of serum hepatitis C RNA in anyone who is antibody-positive
28
When is US usually diagnosed? When is Crohn's usually diagnosed?
UCMost patients are aged 20 to 40 years at diagnosis. Another peak occurs at age 60.CrohnsThe peak age of onset is between 15 and 40 years, and there is a smaller second peak between 60 and 80.
29
What are the causes of jaundice?
30
What tumour marker can be used for pancreatic cancer?
CA19-9
31
What are the causes of pancreatitis?
32
Explain the significance of calcium in pancreatitis?
The lipase released in pancreatitis breaks down the fat laden mesentery (ommentum), to form fatty acids. Fatty acids then combine with calcium (a ubiquitous component in the intercellular fluid) to form a chalky/soapy pancreas (fat necrosis, fat saponification). This process --> hypocalcaemia.
33
What is the clinical picture of pancreatitis?
Severe, constant upper abdominal pain that radiates to the back in 65% of cases builds up over 15-60 minutes.The pt will be learning forward in attempt to alleviate retroperitoneal pain.Nausea, vomiting, anorexia and tachycardia are common.
34
What do you find on examination in pancreatitis?
There is marked epigastric tenderness, but in the early stages guarding and rebound tenderness are absent because the inflammation is principally retroperitoneal.Bowel sounds become quiet or absent as paralytic ileus develops. In some cases, the patient becomes hypoxic and develops hypovolaemic shock with oliguria.Oedema and discolouration of the flanks (Grey Turner’s sign), the periumbilical region (Cullen’s sign) or over the inguinal ligament (Fox’s sign) is a feature of pancreatitis with haemorrhage. These are exceptionally rare signs.Abdominal distension is another common feature of pancreatitis.
35
What are some bedside tests for hypocalcaemia?
36
What key things do you need to keep in mind when interpreting amylase/lipase results?
* The amylase needs to be 3x the upper limit of normal to be pancreatitis, but it is usually much higher than this.
* Amylase is efficiently excreted by the kidneys, and serum concentrations may return to normal within 24-48hours.
* For diagnosis after this time, Lipase remains raised for 7-10 days.
* Serum amylase does not rise as much in hypertriglyceride pancreatitis.
* A lipase to amylase ratio of greater than 5 favours alcoholic pancreatitis rather than gallstone.
* Levels of serum amylase and lipase does not indicate severity.
* Serum amylase is not specific for pancreatitis, elevations can occur in anyone with small bowel obstruction, mesenteric ischaemia, renal insufficiency or tubo-ovarian disease.
37
What is the best imaging modality for pancreatitis?
USSMay show pancreatic inflammation, peri-pancreatic stranding, calcifications, or fluid collections. Use limited as bowel gas obstructs the pancreas 25-35% of the time. Sensitivity in detecting pancreatitis is 62% to 95%. Useful when biliary causes are suspected.CTCan be done to exclude other options if diagnosis ambigous. Will not show signs specific to pancreatitis for 72hours because the complications (e.g. necrosis of the tissue) that show on CT take some time to form.
38
How do we assess the severity of pancreatitis?
39
What is a dermoid cyst?
A dermoid cyst is a cystic teratoma that contains an array of developmentally mature, solid tissues. It frequently consists of skin, complete with hair follicles, and sweat glands. Other commonly found components include: clumps of long hair, pockets of sebum, blood, fat, bone, nails, teeth, eyes, cartilage, and thyroid tissue.
40
Where do venous, arterial and neuropathic ulcers typically occur?
Venous - anywhere from maleoli to kneeArterial - Location over prominent osseous areas and other areas where there is a potential for pressure and skin shearing including between the toes, on the tips of toes, over phalangeal heads, at the lateral malleolus, or sites subjected to repetitive trauma such as contact points with footwear.Neuropathic - Location at areas of repeated trauma such as the plantar metatarsal heads or dorsal interphalangeal joints
41
What is the appearance of arterial vs venous ulcers?
42
What features are typically associated with venous ulcers?
* Leg is warm, normal pulses
* Varicose veins Haemosiderin staining
* Results from extravasation of blood and deposition of haemosiderin in the tissues due to longstanding ambulatory venous hypertension Atrophie Blanche
* White scarred areas surrounded by tiny red spots (enlarged capillaries) Lipodermatosclerosis
* Inflammation of the subcutaneous fat due to CVI. Characterised by woody induration (hardened), thickened and scaly skin. Venous Eczema
* A collective term for lipodermatosclerosis, haemosiderin deposition and athrophie blanche all caused by CVI
43
What are some differences between arterial and venous ulcers?
44
What is this?What is the management?
Seborrhoeic keratoses can easily be removed. The usual reason for removing a seborrhoeic keratosis is your wish to get rid of it. Methods used to remove seborrhoeic keratoses include:
* Cryotherapy (liquid nitrogen) for thinner lesions
* Curettage & cautery
* Laser surgery
* Shave biopsy (shaving off with a scalpel)
45
What are the gross features of melanoma?
ABCDE Signs and SymptomsAsymmetry (is one half different to the other?)Border (regularity, scalloped, poorly defined?)Colour (what colour? >1 colour?)Diameter (> or Elevation / Evolution (is it raised? Is it evolving?)Firm to touchGrowing progressively over more than a month (evolution)May also bleed and ulcerate.
46
What are the gross features of basal cell carcinoma?
“If you can see telangiectasia, non-healing chronic wound / scar and a pearly, white colour when stretched, you know it is a BCC”
* slow-growing
* translucent, pearly white when stretched
* telangiecasia
* papule/nodule
* focal ulceration
* raised, rolled edge
* on the face of the elderly
47
What are the features of a squamous cell carcinoma?
“SCC looks like a red, ulcerated/bleeding or scaly papule, like a non-healing ulcer.”
* Quickly growing (over a few months)
* Painful
* Hyperkeratotic
* Usually nodular
* Crusting, ulceration, scaly, formation of a cutaneous horn
* May be friable and bleed easily and located on sun exposed areas
* Indurated/hard
48
What margins should be used for different melanomas?
In situ melanoma (level 1, 5mm, just in the epidermis): 5mmMelanoma Melanoma 1-4mm: 1-2cmMelanoma >4mm: 2cm
49
What dose of adrenaline do you use for anaphylaxis?
0.01ml/kg of adrenaline 1:1000Repeat every 5 mins
50
What is the initial management of suspected sepsis?
You need to OBLITErate the infectionOxygenBlood culturesLactateIntravenous fluidsTreat (IV antibiotics)Evaluate (monitoring, especially urine output)
51
When you get a page at 3am asking you to come and review Mrs. White because she has a fever, when should you run rather than walk?
52
What is the inheritance pattern of thalassaemia?
Autosomal recessive
53
What is thalassaemia?
A heterogeneous group of genetic disorders of decreased production of normal globin chains leading to anaemia.
54
What investigations would you order to confirm suspected thalassaemia? What would you expect to see?
55
What is the management of thalassaemia?
Trait onlyNothingIntermediaPRN blood transfusionsIron monitoring with PRN chelationChelation may be initiated with desferrioxamineGenetic counselingMajorAs for above but regular transfusionsConsider splenectomyConsider stem cell transplantation
56
What would you look for on exam in suspected thalassaemia?
Symptoms of anaemiaFailure to thrive/short statureJaundice from high RBC turnoverHepatosplenomegaly of extramedullary erythropoiesisLarge head with frontal bossing/chipmunk facies (bone marrow hyperplasia of skull)
57
By definition, what are the clinical features of arthritis?
Inflammation of joints as evidenced byJoint swelling or effusionORDecreased ROMJoint line tendernessPain on movementIncreased warmth
58
A patient has a known pre-existing LBBB. They present today with central chest pain, how do you assess for STEMI?
Sgarbossa criteria
* Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)
* Concordant ST depression > 1 mm in V1-V3 (score 3)
* Excessively discordant ST elevation > 5 mm in leads with a negative QRS complex (score 2). This criterium is sensitive, but not specific for ischemia in LBBB. It is however associated with a worse prognosis, when present in LBBB during ischemia.
A total score of ≥ 3 has a specificity of 90% for diagnosing myocardial infarction.
59
What is electrical alternans?
ECG change seen in severe pericardial effusionWhen consecutive, normally-conducted QRS complexes alternate in height.Produced by the heart swinging backwards and forwards within a large fluid-filled pericardium.
60
What is Conn's syndrome?
Primary hyperaldosteronism / mineralcorticoid excess. Most sources specify that this syndrome refers to hyperaldosteonism caused by an aldosterone-secreting adenoma.
61
What are the causes of hyperaldosteronism?
Primary (aldosterone high, renin low)Aldosterone secreting adenoma (Conn’s)Idiopathic bilateral adrenal hyperplasiaSecondary (aldosterone high, renin high)Inadequate renal perfusion leading to high levels of renin release (heart failure, renal artery stenosis etc.)Renin secreting renal tumour (very rare)
62
Describe the layers of the adrenal cortex and what each layer produces....
63
Explain the renin-angiotensin system....
64
How does hyperaldosteronism affect electrolyte balance?
Sodium retention --> HypernatraemiaFluid retention --> Hypertension (water follows sodium)Potassium excretion --> HypokalaemiaNote that hypokalaemia causes an alkalosis
65
What is the clinical picture of Conn's syndrome?What do you find on investigations?
Note that many patients with Conn’s Syndrome are asymptomatic.Consequences of hypernatraemia
* HTN
* Oedema
Consequences of hypokalaemia
* Muscle weakness / paralysis Nephrogenic diabetes insipidus (pathogenesis super complex)
* And therefore polyuria, polydipsia
Investigations
* ABG (hypokalaemic alkylosis)
* UEC (hypokalaemia, hypernatraemia)
* Serum renin (decreased in Conn’s) Serum aldosterone (increased)
* Renin:aldosterone ratio distinguishes between primary and secondary hyperaldosteronism
* If renin is also high then it is secondary!
* CT of adrenal glands to look for adenoma
66
What is the management of Conn's syndrome?
Surgical removal of tumourMineralocorticoid receptor antagonists (spironolactone)
67
Describe the basic hypothalamus-pituatary-adrenal axis
68
What are the causes of Cushings syndrome?
Exogenous cause:Iatrogenic from excess exogenous glucocorticoids (MOST COMMON)Endogenous cause: ACTH dependent (80%) Caused by a pituitary adenoma (Cushings Disease) which secretes ACTH or
* ACTH secreted from an ectopic source (small cell carcinoma – Lung) ACTH independent
* Excess cortisol secreted from an adrenal carcinoma, a benign adenoma or adrenal nodular hyperplasia
* Rare causes:
* Adrenal carcinoma
69
What are the side effects of corticosteroids?
CUSHINGOIDC - CataractsU - UlcersS – Skin fragility and sleep disturbanceH - HypertensionI - ImmunosuppressionN – Necrosis of the femoral headG – Growth retardationO - OsteoporosisI – Irritability, anxiety and maniaD – Diabetes
70
What are the symptoms of Cushings syndrome?
Central obesityMoon FaceBuffalo humpThin skin, easy bruisingAbdominal striaeOsteoporosis and fracturesHypertensionImpaired glucose tolerance – Diabetes Mellitus ( gluconeogenesis)Predisposition to infections and poor wound healing
71
What investigations would you order for suspected Cushings syndrome?
To diagnose hypercortisolaemia:24 hour urinary free cortisol ---> abnormally high cortisol levelsTo determine aetiology Serum ACTH
* If ACTH low and cortisol high --> adrenal tumour or hyperfunction
* If ACTH high and cortisol high --> ACTH secreting tumour somewhere Dexamethasone suppression test
* Purpose: helps to locate source of ACTH secreting tumour Procedure:
* Serum cortisol is measured before midnight
* Two forms of the test: low and high dose
* Low dose = 2mg dexamethasone given
* High dose = 8mg dexamethasone given
* Serum cortisol is rechecked at 8am. Interpretation
* If ACTH/cortisol levels are suppressed by high but not low dose, Dx is likely to be pituitary adenoma
* Secretion of excess ACTH by pituitary adenoma is usually suppressed by high doses of dexamethasone, but not by low doses
* The key to remember is that low dose dexamethasone will only suppress a normal pituitary, high dose dexamethasone will suppress a pituitary adenoma, but nothing will suppress a SCLC or an adrenal tumor (and you can tell the difference between these to by whether the serum ATCH is high or low)
* Thus if ACTH/cortisol levels are not even suppressed by high doses, Dx is likely ectopic ACTH secreting tumour (like SCC lung cancer) which are not effected by the negative feedback of the dexamethasone An MRI of the pituitary
* If there is a tumour = Cushings disease
72
What is the difference between Cushing's syndrome and Cushings' disease?
Cushings syndrome is a collection of signs and symptoms caused by a chronic inappropriate elevation of free circulating cortisol (hypercortisolaemia).Cushings disease describes hypercortisolaemia (and it’s clinical sequalae) caused by a pituitary adenoma secreting excess ACTH.
73
What are the acute side effects of endogenous or exogenous steroids?
Thrush / oral candidiasis (due to immunosuppression) GI erosions (prostaglandin suppression) “Fluid Shift” causing “Fluid Overload” / HT (AT1 agonism/mimic aldosterone) Acute hyperglycaemia Anxiety, insomnia, mania
74
What is Addison's disease?
Addisons disease aka primary adrenal insufficiency is a disorder that affects the adrenal glands causing decreased production of all 3 adrenocortical hormones (cortisol, aldosterone, and dehydroepiandrosterone).It can be due to adrenal cortex destruction or a decrease in hormone synthesis.90% of the adrenal cortex needs to be destroyed to produce adrenal insufficiency.It may be acute (adrenal crisis) or insidious.
75
What is the aetiology of Addison's disease?
In most cases, Addisons disease is caused by dysfunction of the autoimmune system with antibodies directed against the adrenal cortex.In the developing world it's often caused by TB - tuberculous adrenalitis results from hematogenous spread from active infection elsewhere in the body.
76
What are the symptoms of Addison's disease?
Pigmentation (prominent sign 80-90% of cases)
* This happens from ACTH excess!
* Dull, slaty, grey brown Postural hypotension
* Mineralocorticoid deficiency (80-90% of cases)
* Fatigue/ weakness
* Anorexia
* Dizziness
* Arthralgia/myalgia
* GI symptoms (N+V/ abdominal pain, constipation) – salt craving may be present from loss of mineralcorticoids/aldosterone Women may have significant loss of axillary and pubic hair. Men can still produce testosterone from the testicles so are less commonly affected.
77
What are the investigations (and expected results) of Addison's disease?
BedsideBGL (low due to low cortisol)BloodsFBE (Anemia)UEC (hyponatraemia, hyperkalaemia)Adrenal autoantibodiesMorning serum cortisol (adrenal insufficiency)Serum ACTH levelsACTH and CRH stimulation tests
78
What is a pheochromocytoma?
* a neoplasm composed of cells similar to the chromaffin cells of the mature adrenal medulla
* occur in patients of all ages
* 10% are malignant
* The most clinically important feature of pheochromocytomas is their tendency to produce large amounts of the catecholamine hormones epinephrine (adrenaline) and norepinephrine.
* This may lead to potentially life-threatening high blood pressure, or cardiac arrythmias, and numerous symptoms such as headache, palpitations, anxiety attacks, sweating, weight loss, and tremor.
79
What is the clinical presentation of hypercalcaemia?
Bones, stones, groans and psychic moans
* Bones (increased osteolysis and fractures)
* Stones (renal colic and hypercalcaemic stones) Abdominal groans (anorexia, N&V, constipation, PUD, pancreatitis) Psychic moans (depression, confusion, hallucinations and coma)
Other
* Muscle weakness, malaise, hyporeflexia
* Confusion, apathy, decreased memory
* Nephrogenic diabetes insipidus (polyuria and polydipsia)
80
What are the causes of hypercalcaemia?
* Dehydration
* Drugs including lithium, thiazides and Vitamin D
* If not (1) or (2) it is either primary hyperparathyroidism* or cancer in over 90% of instances
Hypercalcaemia may be associated with malignancies in 2 ways:
* Bony involvement by the tumour may lead to massive osteoclastic activity (osteolytic lesions, think multiple myeloma)
* A variety of tumours release PTH-related peptides
So if hyperparathyroidism is the most common cause, what causes hyperparathyroidism?
Primary hyperparathyroidism: Para-thyroid adenoma (most common)
Secondary hyperparathyroidism: CKD or Vitamin D deficiency causing hypo-calcaemia and therefore a recative hyper-parathyoidism
Tertiary hyperparathyroidism: Development of autonomous PTH hyperplasia after longstanding renal impairment (most commonly after someone is on dialysis or has had a kidney transplant)
81
What ECG changes are seen in hypercalcaemia?
Cardiac Arrhythmia and ECG changes!
* QT shortening
* Prolonged PR
* Widened QRS
* Notched QRS with increased voltage
* AV block --> cardiac arrest
82
What is the management of hypercalcaemia?
There may be no need for intervention in mild hypercalcaemia other than monitoring for complicationsPromote urinary excretion (if CVS and renal function adequate)
* Forced saline diuresis
* Must monitor or replace K and Mg as these will be lost in the urine along with the calcium
HaemodialysisTreatment of choice in CVS or renal compromiseCalcitonin/EDTA bisphosphonatesReduce bone resorbtion and reduce GIT absorption of CalciumEffect in 48 hours and last 15 days
83
What are the causes of hypocalcaemia?
* Factitious result (most common cause from high/low albumin)
* Hyperventilation (resp alkylosis increases binding capacity of albumin)
* Endocrine (Decreased Ca uptake, increased excretion)
* Hypoparathyroidism
* Medullary thyroid carcinoma --> increased calcitonin
* Decreased Vitamin D (decreased GIT calcium absorption) Increased PHOSPHATE (precipitates calcium in serum)
* Tumour lysis syndrome (↑K+ ,↑PO4, ↓Ca++)
* Rhabdomyolysis
* Chronic renal failure
84
What are the clinical features of hypocalcaemia?
Neurological
* Hyperreflexia and seizures
* Paraesthesia of extremities and face (Digital and peri-oral)
* Confusion, hallucinations, dementia
Muscular
* Laryngospasm, stridor, tetany
* Muscle spasm, cramps and tetany
* Chvostek’s (Facial nerve tap….twitch corner of mouth)
* Trousseau (BP cuff on arm for 3mins induces carpopedal spasm)
Cardiac
* Decreased myocardial contractility and heart failure
85
What are the effects of hypocalcaemia on the ECG?
QTc prolongationT wave inversionComplete heart blockTorsades de Pointe
86
What are the causes of thyrotoxicosis?
```
Primary
* Graves’ disease
* Toxic Thyroid Adenoma
* Toxic Multi-nodular goiter
Secondary
* Toxic Pituitary Adenoma/TSHoma
* Early stages of thryroiditis
```
87
Psammoma bodies is the buzz word for?
Papillary carcinoma of the thyroid
88
What is osteomalacia?
A failure of vitamin D to aid the mineralization process --> bone softeningBone matrix is intact, just de-mineralised c.f. osteoporosis/ osteopeania in which the matrix abnormalRickett's shares the same underlying pathopysiology but is the diagnosis in kids who's growth plates have not yet fused
89
What most commonly causes osteomalacia and Rickets?
Osteomalacia Most common cause = Vit D deficiency
* Vit D, phosphate and calcium deficiency, most often related to dietary deficiency, lack of sunlight or malabsorption.
* Renal osteodystrophy
Rickets
* Dark skinned babies/children due to their decreased Vitamin D levels and
* Infants breast fed from Vit D deficient mothers
90
What is the clinical presentation of osteomalacia?
* Pathological fractures
* Diffuse bone pain
* Proximal muscle weakness/wasting which can lead to waddling gait and difficulty climbing stairs* Risk factors for Vit D deficiency:
* Vit D deficient diet
* Low sunlight exposure
* Malabsorption syndromes
* Anticonvulsent use
* Low phosphate causes proximal myopathy
91
What is the clinical presentation of Ricket's?
Most commonly at sites of rapid bone growth eg: distal forearm
* Widening of the bones at the wrists and knees
* Curving of bones
* Lumpy joints (traction epiphyses)
* Fontanels slow to close
* Bowing of the legs
* Spine deformities
* Fractures
* Bone pain and dental abnormalities
92
What do you find on investigation of osteomalacia/ricket's?
*PTH causes retention of Ca and excretion of phosphate in the kidneysDEXA scan will usually show osteopenia rather than osteoporosisCheck UEC to rule out renal osteodystrophy
93
What is the management of Ricket's/osteomalacia?
* Treat the cause
* Nutritional deficiencies can be solved with replacement --> Calcium carbonate + colecalciferol (Ostevit)
* If hyperphosphataemia – treat by avoiding milk, cheese and eggs OR give phosphate binders
94
Explain the pathogenesis of renal osteodystrophy.
Two mechanisms:
* Reduced production of the active form of vitamin D --> hypocalcaemia (as vitamin D facilitates calcium absorption from the GIT)
* Phosphate is not excreted --> hyperphosphataemia. Excess phosphate binds to calcium --> hypocalcaemia
NB. Both of these processes cause secondary hyperparathyroidism (but this is a normal physiological reaction, and doesn’t itself cause renal bone disease)
95
What is Paget's disease?
A chronic bone disorder characterized by increase bone resorption by abnormal osteoclasts and subsequent bone remodeling. This unbalanced process may lead to osseous deformities, structural weakness, altered joint biomechanics, and eventually bone fractures and cranial/spinal nerve compressions.It may be either monostotic (25%) involving only 1 bone (frequently the femur) or polyostotic (75%) involving more than one bone
96
What is the classic presentation of Paget's disease?
Patients are usually asymptomatic but may complain of:severe pain in long bones + facial areasPain may be secondary to pathological fractures that occur as a result of weakened bones, most commonly femurl/pelvis or tibia + flat bones (skull).May present as prognathism, hearing/vision loss, loosening of teeth or disturbances in chewing if facial bones are affected. Can also feature Frontal bossing and bowing of femur.
97
What would you find on investigation of Paget's disease?
Characteristic Xray:1. Expansion of bone2. Cortical thickening3. Prominent trabeculae ↑ALP, normal Ca, ↑ ESR/CRP, normal Vit D
98
What would you find on investigations of renal bone disease/renal osteodystrophy?
99
What is osteoporosis?
A complex disease causing decreased bone strength and increased susceptibility to fracture due to reduced bone mineral density (DEXA detectable) AND abnormal bony architecture (DEXA un-detectable).
100
What will you find on investigation of osteoporosis?
DEXA scores are reported as "T-scores" and "Z-scores."The T-score is a comparison of a person's bone density with that of a healthy 30-year-old of the same sex.The Z-score is a comparison of a person's bone density with that of an average person of the same age and sex.Lower scores (more negative) mean lower bone density:A T-score of -2.5 or lower qualifies as osteoporosis*.A T-score of -1.0 to -2.5 signifies osteopenia, meaning below-normal bone density without full osteoporosis.
101
What are the risk factors for osteoporosis?
* Female
* Older age
* Early menopause
* Low BMI
* Immobilisation
* Smoking
* ETOH
* Low Ca intake
* Low Vit D intake
* Inadequate sun exposure
* Steroid ise
* Anti-convulsant use
* Cushings
* HyperPTH
* Hyperthyroidism CKD
102
What are the indications for pharmacotherapy Tx of osteoporosis?
103
What is the full management of osteoporosis?
BasicEducation and reassurancePlace and personGP managedInvestigate and confirm diagnosis
* FBE
* UEC (rule out renal osteodystrophy)
* LFTs (rule out chronic liver dz)
* CMP (Hypocalcaemia? Primary hyperparathyroidism (high Ca, low phosphate))
* Parathyroid hormone levels
* Vit D levels
* TSH (hyperthyroidism?)
* Serum and urine electrophoretogram and immunoelectrophoretogram (multiple myeloma)
* Anti-TTG and IgA (coeliac)
* DEXA scan
Non invasive
* Quit smoking, reduce alcohol
* Calcium and vitamin D
* Weight bearing exercise
* Physio and OT to prevent falls
DefinitiveIndications for pharmacotherapy:
* Minimal trauma fracture
* >70 yrs and T score -3.0 or lower
* T score less than -1.5 and prolonged steroids
Options: Bisphosphonates:
* Aledronate, oral, weekly, up to 10 years
* Zoledronic acid, IV, yearly for 3 years
* SERM – Raloxifene
* Monoclonal antibody – Denosumab
* Teriparatide (PTH analogue)
* Strontium ranelate
What do you need to know about bisphosphonates:
* Significantly reduces the risk of # and complications of OP
* Do not eat or drink before taking the drug
* Take once a week, standing up with a full glass of water.
* Take the tablet whole, do not crush or chew.
* Remain standing up for 30mins after taking.
* Do not eat, drink or lie down for 30 mins after taking Risks
* Oesophageal irritation
* Upper GI ulcers
* Musculoskeletal aches and pains
* Osteonecrosis of the jaw (rare)
* Atypical femoral stress fractures (rare)
* Delays bone healing if there is a #
104
When you discover hypertension, what should you do before prescribing an antihypertensive?
1) Is the HTN primary or secondary?ABCDE
* Apnea, Aldosteronism
* Bruits / Bad Kidneys
* Catecholamines, Cushings, Coartation, Calcaemia Drugs
* Corticosteroids
* OCP
* Decongestants (pseudoephedrine)
* ETOH
* NSAIDs
* Oestrogen
* Psych drugs – MAOi, Lithium, Clonidine
* Endocrine (hyperthyroidism)
2) How bad is has it been? - assess for end organ damage Heart
* LVH (ECG, TTE/TOE) Kidneys
* Albumin:creatnine
* Protein:creatnine
* eGFR Eyes
* Fundoscopy Vascular Auscultate for bruits
* U/S or angiogram
3) How bad might it be in the future? - assess overall CV risk
105
What medications commonly cause hypertension?
CorticosteroidsOCPDecongestants (pseudoephedrine)ETOHNSAIDsOestrogenPsych drugs – MAOi, Lithium, Clonidine
106
What tests (and results) can you use to diagnose T2DM?
* FBG ≥7.0 mmol/L (on two separate occasions)
* 2 hour postprandial ≥11.0 mmol/L on OGTT (on two separate occasions)
* HbA1c ≥6.5% (48 mmol/mol) (on two separate occasions) - ALTHOUGH THIS ISN'T CURRENTLY FINDED BY MEDICARE
107
Describe the pathophysiology of DKA...
In the absence of insulin, glucose remains in the bloodstream and is unable to be taken up into cells à stimulates metabolism of other substrates, notably fatty acids, to produce glucose à ketone bodies are produced.Ketone bodies are acidic and produce a Metabolic ACIDOSIS.Severe hyperglycaemia can exacerbate the classical triad of symptoms (polyuria, polydipsia, polyphagia) and patients are severely dehydrated.The hyperglycaemia causes a profound osmotic diuresis leading to dehydration and electrolyte loss, particularly of sodium and potassium. Potassium loss is exacerbated by secondary hyperaldosteronism as a result of reduced renal perfusion.
108
Discuss the significance of Na in DKA....
In hyperglycaemia the osmolarity of ECF rises, causing a shift of ICF water into the ECF. This has a dilutional effect on extracellular [Na] leading to an apparent hyponatraemia. In fact, total body [Na] is normal, it has just been diluted. To compensate for this, when a patient is hyperglycaemic use the following formula to calculate what the [Na] actually would be, if not for the hyperglycaemia: Corrected (i.e. actual) Na = measured Na + 0.3 (glucose - 5.5) mmol/li.e. 3 mmol/l of sodium to be added for every 10 mmol/l of glucose above 5.5 mmol/l. If Na is > 160 mmol/l, discuss with senior doctor.If sodium does not rise as the glucose falls during treatment or if hyponatraemia develops, it usually indicates overzealous volume correction and insufficient electrolyte replacement. This may place the patient at risk of cerebral oedema.
109
What is the emergency management of DKA?
SPIDERS – IV SalineP – PotassiumI – InsulinD – DextroseE – Eating – Nil by mouth.R – Reason – find a reason – monitor compliance.
110
What are the macro and microvascular complications of DM?
Microvascular complications:RetinopathyNephropathyNeuropathyMacrovascular complications:Peripheral vascular disease (PVD)Cardiovascular (MI)Cerebrovascular (CVA/TIA)
111
What are the common manifestations of diabetic neuropathy?
* Glove and stocking sensory neuropathy
* CN III nerve palsy --> diplopia
* Mononeuropathy multiplex (femoral nerve)
* Polyneuropathy Autonomic neuropathy.
* postural hypotension
* urinary incontinence
* erectile dysfunction
* gastroparesis, nausea, bloating and diarrhea
112
What do you know about metformin?
MOA
* Reduces glucose absorption by the GI tract
* Reduces gluconeogenesis by the liver
* Increases glucose metabolism by cells Dose
* 500 mg orally once daily initially, increase by 500 mg/day increments every week (do this to reduce side effects)
* Maximum 1000 mg twice daily Side effects:
* Flatus, Diarrhoea, Nausea Note that Metformin can induce a lactic acidosis (1/30,000 pts per year)
* Poor kidney function means that you will accumulate metformin --> lactic acidosis.
* Metformin should therefore be ceased before using contrast for imaging. As contrast can --> renal failure. It is better to transiently give a patient hyperglycaemia, than induce a lactic acidosis. Contraindications
* Cr > 150, eGFR
* Liver failure
* EtOH abuse
* Cardiac or resp failure
* Sepsis
* Dehydration
* Age >80
* Withold w acute illness, surgery and before/after radiocontrast
113
After metformin, what is the next step pharmacotherapy of T2DM? How does it work?
Sulphonylureas Stimulate insulin release from beta pancreatic cells. Therefore only effective when pancreas has functioning B cells.Complications: weight gain and hypoglycaemia
114
What is the T2DM equivalent of DKA?What are the criteria for diagnosis of this condition?
* Severe hyperglycaemia (>30 mmol/L)
* Severe hyperosmolality (serum osmolality > 320 mOsm/kg)
* Dehydration
In the absence of significant hyperketonaemia ( 7.3, bicarbonate > 15 mmol/L).
As with DKA, there is glycosuria, leading to an osmotic diuresis, with loss of water, sodium, potassium and other electrolytes.However, in HHS, hyperglycaemia usually develops over a longer period (a few days to weeks), causing more profound hyperglycaemia and dehydration (fluid loss may be 10–22 litres in a person weighing 100 kg).
115
What are the causes of post-op fever?
WATER, WIND, WIZZ, WALK, WOUND, & WEIRD DRUGSWATER = IV site infectionsWIND = pneumoniaWIZZ = UTIWALK = deep vein thrombosisWOUND = surgucal wound infectionWEIRD DRUGS = drug induced fever
116
What is the epidemiology of SLE?
Some 90% of affected patients are female and the peak age at onset is between 20 and 30 years.High prevalence in those of south east Asian descent.
117
In one sentence, what is the aetiology/pathyphys of SLE?
Lupus is an autoimmune disease, in which the body loses tolerance to itself due to both genetic and environmental factors.Shows a relapsing remitting pattern.
118
What are the diagnostic criteria for SLE?
A RASH POINts MD (need >4 for Dx)Arthritis Renal disease (proteinuria, cellular casts) ANA (positive antinuclear antibody) Serositis (pleurisy or pericarditis) Haematological disorders (haemolytic anaemia or leucopenia or lymphopenia or thrombocytopenia) Photosensitivity Oral ulcers Immunological disorder (positive anti-DNA, anti-Sm, false positive serological test for syphilis) Neurological disorders (seizures or psychosis, in the absence of other causes) Malar rash Discoid rash
119
What are the relative and absolute contraindications to hormonal contraceptives?
HOMESICKHeadache / HypertensionObesityMedications (some antivirals/ABx)Embolism / Thrombus / Clotting disordersStrokeIHDCancer (Breast, Endometrial)Kids (ie. parity) / Breastfeeding
120
What is the function of the appendix?
It is gut mucosa-associated lymphoid tissue. It may also have a role in storing normal gut flora for replenishment after a bout of severe diarrheoa or illness washes out the normal flora.
121
What do you know about Guillain-Barre syndrome?
Definition: It is an idiopathic, autoimmune motor neuropathy. Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) is the most common form in western countries and accounts for 85% to 90% of casesEpiHappens to all ages and genders, it is the most common cause of acute flaccid paralysis in children.Two-thirds of patients have had infections within the 6 weeks before symptom onset, most commonly URTI and gastroenteritis. The acute infectious illness is usually viral Presentation: Progressive symmetrical muscle weakness usually affecting lower extremities before upper extremities and proximal muscles before distal muscles accompanied by paraesthesias in the feet and hands. The paralysis is typically flaccid with areflexia.Management: Supportive care, mechanical ventilation if required, plasma exchange and IVIGPrognosisThe overall prognosis of GBS is good, with approximately 85% of survivors making a good functional recovery. Mortality of 20% has been shown in ventilated patients.
