DPD 5 - Acute, Endo, Breast + Haem Flashcards

1
Q

A 24 y/o man presents w/ short onset breathlessness + facial swelling after a Chinese takeaway. What is the Dx?

A

Anaphylaxis

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2
Q

A 24 y/o man presents w/ short onset breathlessness + facial swelling after a Chinese takeaway. A Dx of anaphylaxis is made. What is the first step in management?

  1. IM adrenaline
  2. IV adrenaline
  3. IM hydrocortisone
  4. IV hydrocortinsone
  5. IV fluids
A

IM adrenaline

Hydrocortisone + fluids are part of Mx but not first step

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3
Q

A 45 y/o man presents w/ cough, breathlessness + recent travel. O/E: Coarse crepitations + bronchial breathing. He has hyponatraemia + deranged LFTs. What is the most likely Dx?

A

Community acquired pneumonia

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4
Q

What is the Tx for CAP?

A

Amoxicillin - covers Strep. pneumonia

Macrolide - e.g. Clarithromycin to cover for atypical pneumonia

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5
Q

A 45 y/o man presents w/ cough, breathlessness + recent travel. O/E: Coarse crepitations + bronchial breathing. He has hyponatraemia + deranged LFTs. A Dx of CAP has been made and he is given amoxicillin. What antibiotics would you prescribe in addition to amoxicillin?

  1. Cefuorxime
  2. Clarithromycin
  3. Co-amoxiclav
  4. Tazocin
  5. Vancomycin
A

Clarithromycin - macrolide to cover for atypical pneumonia. It has good bioavailability so given orally 250 mg twice daily usually for 1-2 weeks

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6
Q

What antibiotic would you use to treat HAP?

A

Tazocin - Gram negative organisms e.g. Klebsiella. 4.5g every 8 hours

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7
Q

What antibiotic would you use to treat MRSA?

A

Vancomycin

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8
Q

Name 3 atypical organisms in pneumonia

A

Mycoplasma pneumoniae
Chlamydia pneumoniae
Legionella pneumoniae - assoc. w/ bodies of water e.g. AC conditioning, plumbers etc

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9
Q

A 50 y/o man presents w/ dyspepsia + weight loss. Ix: Hb 70; MCV 70. What test would you request?

  1. Abdominal CT
  2. Abdominal USS
  3. Erect CXR
  4. Colonoscopy
  5. OGD (Gastroscopy)
A

OGD as the symptoms suggest upper GI due to microcytic anaemia + dyspepsia (impaired digestion) + weight loss (red flag). If NAD then do colonoscopy.
Erect CXR done if there is perforation - pt will present w/ diffused abdo pain, rigidity, guarding, same w/ abdo CT
Abdo USS - next Ix in patients w/ deranged LFTs (common bile ducts to look for obstruction)

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10
Q

What Ix would you do if you found microcytic anaemia? (x 3)

A
OGD + Colonscopy: investigate top + tail; when to do which depends on upper/lower GI symptoms
Haematinics: iron studies, ferritin, folate/B12
Coeliac screen (TTG ab + duodenal biopsy - this is diagnostic)
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11
Q

What kind of protein is ferritin and when will it be raised?

A

Ferritin is an acute phase protein and will be raised in infection, inflammation + malignancy therefore iron deficiency anaemia + pneumonia may have normal ferritin as it is induced by infection.

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12
Q

What kind of protein is folate and when will it be raised?

A

Folate is an acute phase protein. Infection + malignancy will cause increased folate.

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13
Q

What confirms diagnosis of coeliac disease + what will be seen?

A

Duodenal biopsy

Villous atrophy, crypt hyperplasia

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14
Q

What is coeliac disease?

A

Systemic AI disease triggered by dietary gluten peptides found in wheat, rye, barley + related grains. Presentation: diarrhoea, bloating, abdo pain/discomfort, failure to thrive, iron deficiency microcytic anaemia, osteoporosis, dermatitis herpetiformis

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15
Q

What is the Tx for coeliac disease?

A

Strict, lifelong gluten-free diet

Vit D supplements for vit D deficiency

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16
Q

A 70 y/o man presents w/ bloody diarrhoea. Stool micro + culture -ve. Stool C. diff toxin: -ve. What is the most likely diagnosis?

  1. Infective colitis
  2. Ischaemic colitis
  3. UC
  4. Appendicitis
  5. Gastroenteritis
A

Ischaemic colitis - typically older patients affecting smaller vessels as opposed to mesenteric ischaemia
Unlikely to be infective colitis due to -ve stool culture + -ve toxin. UC typically younger patients (30-40s).

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17
Q

What are the 5 organisms that most commonly cause infective colitis therefore bloody diarrhoea?

A
CHESS organisms
Campylobacter
Haemorrhagic E. coli (0157) - assoc. w/ haemolytic uraemic syndrome
Entomoaeba histolytica
Salmonella
Shigella
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18
Q

A 40 y/o man presents w/ palpitations that started 4 hours ago. ECG: AF. How would you treat him?

  1. Adenosine
  2. Amiodarone
  3. Digoxin
  4. Metoprolol
  5. DC cardioversion
A

DC cardioversion as he is presenting < 48 hours
Adenosine is for SVT; Amiodarone is for broad complex tachycardia (VT) but works on all arrhythmias (often 2nd/3rd line); digoxin + metoprolol is for rate control

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19
Q

What is the management of AF that is <48 hours onset?

A

DC cardioversion to revert back to sinus rhythm or chemical cardioversion with flecainide

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20
Q

What is the management of AF that is >48 hours onset?

A

Anticoagulate w/ LMWH + rate control with BB/digoxin

After 3-4 weeks, DC cardioversion to prevent clot dislodging

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21
Q

A sign is seen on a pt’s abdomen - the direction of flow in the veins below the umbilicus is towards the legs. What is the name of this clinical sign?

  1. Trousseau’s sign
  2. Virchow’s node
  3. Caput medusa
  4. Troisier’s sign
  5. Grey Turner sign
A

Caput medusa - sign of portal hypertension

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22
Q

What does Trousseau’s sign indicate?

A

Hypercalcaemia - carpopedal spasm w/ BP cuff
OR
Sign of thrombophlebitis in Pancreatic cancer

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23
Q

What does Virchow’s node indicate?

A

Supraclavicular lymph node indicated gastric cancer

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24
Q

What does Troisier’s sign indicate?

A

Enlargement of left supraclavicular lymph node due to secondary involvement

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25
Q

What does Grey Turner’s sign indicate?

A

Bruising assoc. w/ pancreatitis (retroperitoneal haemorrhage)

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26
Q

A 20 y/o boy presents w/ recent diarrhoea + malaise. Hb 70; Cr 300. Arrows on blood film point to fragmented cells. What does this indicate?

  1. Codocytes
  2. Eliptocytes
  3. Lymphocytes
  4. Schistocyte
  5. Spherocyte
A
Schistocyte - red cell fragment
Not codocyte (target cell) seen in hyposplenism
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27
Q

What are the signs of portal hypertension?

A
Presents w/ signs of decompensated liver disease:
Encephalopathy
Ascites
SBP
Variceal bleed
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28
Q

What is the pathophysiology in MAHA?

A

Lots of tiny clots in small vessels (microangiopathic) which narrow small vessels. As RBCs pass through these narrow vessels they break up - haemolysis. This is why you see schistocytes in MAHA + low Hb

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29
Q

What is the pathophysiology in DIC?

A

Widespread intravascular coagulation - constant making and breaking of clots. Paradoxically prone to bleeding as clotting factors being used up

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30
Q

What are the levels of (1) platelets + fibrinogen (2) PT/APTT (3) D-Dimer/fibrin degradation products in DIC?

A
  1. Decreased platelets + fibrinogen as they used up to make tiny clots + fibrinogen is turned into fibrin as RBC trapped in fibrin strands
  2. Increased PT/APTT as clotting factors used up
  3. Increased D-dimer/fibrin degradation products due to fibrinolysis
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31
Q

Which part of the coagulation pathway does (1) PT and (2) APTT refer to?

A
  1. PT refers to the extrinsic pathway

2. APTT refers to the intrinsic pathway

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32
Q

How does Haemolytic Uraemic Syndrome present?

A

Haemolysis - decreased Hb and increased bilirubin causing pre-hepatic jaundice
Uraemia
Decreased platelets
Abdo pain
Assoc. w/ E coli 0157 in children commonly

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33
Q

What is Thrombotic Thrombocytopenic Purpura (TTP)?

A

HUS + Fever + neurological manifestations e.g. seizure

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34
Q

What causes haemolytic anaemia (x2)?

A

Hereditary - defect in RBC membrane (hereditary spherocytosis); enzyme deficiency (G6PD deficiency, pyruvate kinase deficiency); haemoglobinopathy (sickle cell disease, thalassaemia)
Acquired - AI e.g. SLE; drugs; infection; MAHA

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35
Q

A CXR shows circular folds in the small bowel, what does this show?

  1. Adhesions
  2. Haustra
  3. Large bowel
  4. Stomach
  5. Valvulae conniventes
A
Valvulae conniventes (= Kerckring folds)
Haustra is a feature of large bowel
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36
Q

What is the Tx for small bowel obstruction?

A

NBM

Drip + suck (IV fluids, NG tube)

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37
Q

A 60 y/o man presents w/ confusion, cough and no postural hypotension. Na 120 (low); K 4; TFT + Short Synacthen test is normal. Urine Na+ 40; Urine osmolality 400. What test would you request next?

  1. Brain MRI
  2. CT abdo
  3. CXR
  4. Lung function test
  5. OGD
A

CXR - look for lung abnormality; if normal then do CT head and then MRI brain
If hyponatraemic, firstly must assess volume status: hypovolaemic, euvolaemic, hypervolaemic
Cause of all low sodium - increased extracellular water - secrete excess ADH (makes you reabsorb water)

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38
Q

What is the classification of ADH?

A

Appropriate ADH: hypovolaemia due to diarrhoea + vomiting (physiological response to stimulus)
Inappropriate ADH: Tumour that secretes ADH

39
Q

What single Ix best indicates hypovolaemia?

A

Urine sodium
Kidneys will try its best to reabsorb sodium giving low urine sodium
Low urine sodium in a pt w/ D+V is a good indicator of hypovolaemia (only valid if patient is not on diuretics)

40
Q

What is the classification of hyponatraemia?

A

Hypovolaemia
Euvolaemia
Hypervolaemia

41
Q

What are the causes, presentation + Tx of hypovolaemia?

A

Causes: diarrhoea, vomiting, diuretics
Presentation: Postural hypotension, tachycardia, reduced skin turgor, dry mucous membranes .
Low urine Na+ - must measure off diuretics; kidneys will reabsorb more Na+
Tx: Fluids 0.9% saline

42
Q

What are the causes, presentation + Tx of euvolaemia?

A

Causes: Endocrine - SIADH, Hypothyroidism, Adrenal insufficiency
Presentation: TFTs; short synacthen test (normal: increased cortisol). Low plasma osmolality due to decreased Na+. Increased plasma osmolality due to increased SIADH
Tx: Fluid restriction

43
Q

What are the causes + presentation of hypervolaemia?

A

Cause: cardiac failure, cirrhosis, nephrotic syndrome
Presentation: Signs of fluid overload e.g. peripheral oedema; low urine Na+ (due to reduced bloodflow to kidney - increased renin + ATN - increased aldosterone - increased Na + reabsoprtion. Increased JVP

44
Q

What is the cause of all hyponatraemia?

  1. Too much water
  2. Too much salt
A

Too much water (NOT a salt problem)
Majority of cases due to increased ADH appropriately or inappropriately i.e. SiADH - Too much water reabsorption therefore decreased Na+
Rarer causes include excess water intake, sodium free irrigation solutions e.g. used in TURP (transurethral resection of prostate

45
Q

What are the causes of SIADH? (x4)

A

Think brain, lung and pill

  1. CNS pathology - Stroke, tumour, abscess
  2. Lung pathology - Pneumonia, PE, lung cancer
  3. Drugs - SSRI, TCA, opiates, PPIs, carbamazepine
  4. Tumours - Ectopic ADH
46
Q

What is the management of hyponatraemia?

A

Treat the cause
Do not correct Na+ too rapidly (no more than 8mmol/24 hours) as there is a risk of cerebral pontine myeolysis
If fitting or decreased GCS - 3% Hypertonic saline

47
Q

A 35 y/o man presents w/ sweating and weight loss. His nails are coming off from his nailbed, what is the name of this sign?

  1. Beau’s lines
  2. Nail pitting
  3. Koilonychia
  4. Onycholysis
  5. Leukonychia
A

Onycholysis = separation from nailbed. Causes: trauma, thyrotoxicosis, fungal infection, psoariasis
Beau’s lines are alternating dark and white lines due to repeated arrest + growth e.g. recurrent chemotherapy
Nail pitting is a feature of psoriasis; koilonychia is spoon shaped nails which is a feature of iron deficiency. Leukonychia is a sign of hypoalbuminaemia, liver disease

48
Q

A 20 y/o woman presents w/ abdo pain + vomiting. She has T1DM, CBG: 20, Venous pH 7.20. What is the next most appropriate next step?

  1. Capillary ketone
  2. FBC
  3. HbA1c
  4. LFTs
  5. CRP
A

Capillary ketone - check for DKA

49
Q

What are the microvascular complications of diabetes?

A

Retinopathy
Nephropathy - U&Es, urine albumin, creatinine ratio (ACR)
Neuropathy (foot ulcer)

50
Q

What are the macrovascular complications of diabetes?

A

MI
Stroke
Peripheral vascular disease

51
Q

What are the metabolic complications of diabetes?

A

DKA
HHS
Hypoglycaemia

52
Q

A 26 y/o man presents w/ chest pain. He smokes 5 a day and on auscultation a ‘scratching sound’ can be heard. An ECG shows widespread ST elevation in multiple leads. What is the most likely diagnosis that is supported by his ECG?

  1. Anterolateral MI
  2. Inferior MI
  3. NSTEMI
  4. Pericarditis
  5. Posterior MI
A

Pericarditis

53
Q

A 60 y/o woman presents w/ collapse. BP: 120/70 mmHg and there is no postural drop. HS: S1 + S2+ ESM. Her ECG shows deep S waves in V1 + deep R waves in V6. What is the most likely diagnosis?

  1. Left atrial hypertrophy
  2. Left ventricular hypertrophy
  3. Right atrial hypertrophy
  4. Right ventricular hypertrophy
  5. NAD
A

Left ventricular hypertrophy - the ESM indicates aortic stenosis + the voltage criteria = Deep S in V1 + Tall R in V6; the LVH may be due to an aortic stenosis

54
Q

A 40 y/o man presents w/ loin pain. CRP normal and urinalysis: blood +++. What investigation would you request?

  1. Abdo X ray
  2. Abdo USS
  3. CTKUB
  4. CT with contrast
  5. MR angiogram
A

CT-KUB (non-contrast, unenhanced) is gold standard for acute renal colic to look for stone causing obstruction.

55
Q

What are the DDx of loin pain w/ haematuria?

A

Pyelonephritis: rigors, painful when tapping renal angle, increased CRP
Renal colic

56
Q

A 50 y/o man presents w/ hypercalcaemia, low PTH, backache + normal ALP. What is the most likely Dx?

  1. Bone metastases
  2. Multiple myeloma
  3. Osteoporosis
  4. Primary hyperparathyroidism
  5. Secondary hyperparathyroidism
A

Multiple myeloma - in myeloma, plasma cells produce paraprotein monoclonal Ig + supress osteoblasts which make ALP
Increased Ca with low PTH would indicate malignancy, sarcoidosis, myeloma. Backache can occur in malignancy or myeloma. Normal ALP indicates myeloma as ALP would be high in malignancy.

57
Q

What does a high Ca2+ and high PTH indicate?

A

Hyperparathyroidism

58
Q

What does a high Ca2+ and a low PTH indicate?

A

Malignancy (bone mets), sarcoidosis, myeloma - something else other than PTH is driving the calcium (PTH-related peptide)

59
Q

Where is ALP made?

A

Liver and Bone (osteoblasts)

60
Q

What does an increased ALP indicate?

A

Obstructive liver disease, bone disease (malignancy, fracture, Paget’s disease)

61
Q

What is the definition of multiple myeloma?

A

Plasma cell dyscrasia (abnormal state) characterised by terminally differentiated plasma cells, infiltration of the bone marrow by plasma cells + presence of a monoclonal Ig or Ig fragment in serum +/or urine. Usually assoc. w/ osteolytic bone disease, anaemia + renal failure

62
Q

What are the symptoms of multiple myeloma?

A
Think CRAB
Elevated Calcium 
Renal insufficiency (creatinine > 173mmol/L)
Anaemia
Bone pain/disease (lytic or osteopenic)

M-protein in serum >30 g/L and/or bone marrow clonal plasma cells >10%

63
Q

What Ix would you do for multiple myeloma?

A

Serum/urine electrophoresis is gold standard + diagnostic test - paraprotein spike + light chain urinary excretion > 1g/day (Bence Jones proteins)
Can also do a skeletal survery and bone marrow aspirate + biopsy

64
Q

A 23 y/o woman presents w/ a 1cm smooth, mobile breast lump. What is the most likely Dx?

  1. Basal cell carcinoma
  2. Ductal carcinoma
  3. Fat necrosis
  4. Fibroadenoma
  5. Galactocoele
A

Fibroadenoma - most common cause of benign, smooth, mobile breast lump in women.
Fat necrosis is assoc. w/ trauma + galactocele is commonly in pregnancy, post partum = retention of cyst containing milk usually located in the mammary gland

65
Q

What does a cavitating lesion on a CXR indicate?

A

Infection - S. aureus, TB, Klebsiella in alcoholics
Inflammation - Granulomatosis w/ polyangiitis (Wegener’s assoc. w/ cANCA), RhA
Infarction - PE
Malignancy - squamous cell carcinoma which can secrete ACTH/ADH and is most commonly found in the central lung

66
Q

What does interstitial shadowing indicate on CXR?

A

Fluid or pus e.g. heart failure

67
Q

How does a pleural effusion present on a CXR?

A

Homogenous white

68
Q

What does reticulonodular shadowing indicate on CXR?

A

Reticulonodular shadowing

69
Q

What does bilateral hilar lymphadenopathy indicate?

A

Sarcoidosis

70
Q

What are the DDx for a pulmonary cavitating lesion?

A

Pneumonic: CAVITY
Cancer: bronchogenic carcinoma most often SCC; cavitary pulmonay metastasis also most often SCC
Autoimmune: granulomas form e.g. in Wegener granulomatosis and rheumatoid arthritis (rheumatoid nodules)
Vascular: bland and septic pulmonary emboli
Infection: pulmonary abscess or pulmonary TB
Trauma: Pneumatoceles (found in infancy) = intrapulmonary air-filled cystic spaces
Youth: CPAM = Congenital Pulmonary Airway Malformation; pulmonary sequestration; bronchogenic cyst

71
Q

A 35 y/o woman presents w/ ankle oedema. Recent Echo NAD. U+Es normal; ALT, AST, ALP normal. Albumin - 15 (low). What test would you like to order?

  1. Coronary angiogram
  2. Renal USS
  3. Troponin
  4. Urinalysis
  5. Repeat LFTs
A

Urinalysis to look for losing protein in urine - low albumin is a cause of ankle oedema. Peripheral oedema indicates cardiac failure or nephrotic syndrome. The echo rules out heart failure therefore ankle oedema likely to be due to low albumin.

72
Q

What is nephrotic syndrome?

A

Proteinuria, Oedema + Hypoalbuminaemia
Due to increased permeability of GBM to protein. Other features include: prone to thromboembolic disease e.g. renal vein thrombosis because they lose endogenous anticoagulants in urine

73
Q

What is nephritic syndrome?

A

HTN + Proteinuria + Haematuria
Due to pores in podocytes are large enough to allow protein and RBCs to pass into urine. May also be red cell casts in urine indicative of glomerular damage. Other features include low urine output due to decreased renal function

74
Q

What is membranous glomerulonephritis?

A

Non-proliferative glomerulonephritis. Thickening of glomerular basement membrane from immune complex deposition. Can be primary or secondary to malignancy, infection, immunological disease (SLE, RhA, Sjogren’s) or drugs (gold, penicillamine)

Diffusely thickened GBM due to subepithelial deposits. Spikes and Dome seen on silver stain

75
Q

What is minimal change glomerulonephritis?

A

Increased cytokine damage to foot process of podocytes of glomerulus in kidney. More commonly seen in children.
Causes: idiopathic, drugs (NSAIDs, lithium), paraneoplasms (Hodgkin’s lymphoma)
Does not cause renal failure

76
Q

What is the Ix for minimal change glomerulonephritis?

A

Light microscopy is NORMAL
Electron microscopy shows effacement of podocyte foot processes
Immunoflorescence - negative as not due to immune complex

77
Q

What is focal segmental glomerulosclerosis (FSCS)?

A

Chronic pathological process caused by injury to podocytes in the renal glomeruli, affects only part of the glomeruli

78
Q

How can focal segmental glomerulosclerosis present?

A

Oedema, foamy urine, HTN, Muehrcke’s line = white banding on nails due to hypoalbuminaemia, xanthelasma + xanthoma

79
Q

How can focal segmental glomerulosclerosis be diagnosed?

A

Focal sclerosis

80
Q

What is IgA nephropathy?

A

Proliferative flomerulopathy (nephritic syndrome) which often presents as asymptomatic non-visible haematuria within days of an infection. Increased BP + proteinuria.

81
Q

What is the Ix for IgA nephropathy?

A

Renal biopsy: IgA deposition in mesangium

82
Q

How does Henoch-schonlein purpura present?

A

Purpuric rash, abdo pain, joint pain, GI bleeding. Affects multi-systems including skin, GI tract, joints + connective tissue.

83
Q

What is post-streptococcal glomerulonephritis?

A

Occurs weeks after a throat/skin infection as streptococcal antigen deposits in glomerulus –> immune complex formation and inflammation (Type 3 hypersensitivity).

84
Q

What is the Ix for post-streptococcal glomerulonephritis?

A

Increased anti-streptococcal Ab titre

Increased anti-DNAse B

85
Q

What is membranoproliferative flomerulonephritis?

A

Divided into:
Immune complex associated (Type 1): increased or abnormal immune complexes deposited in kidney + activate complement.
C3 glomerulopathy - due to genetic or acquired defect in alternative complement pathway

86
Q

What is rapidly progressive glomerulonephritis?

A

Nephritic syndrome characterised by proliferation of epithelial cell into crescent shape. Any aggressive GN rapidly progressing to renal failure over days or weeks - crescent formation by macrophages + epithelial cells, which fills up Bowman’s space + causes rupture.

87
Q

What Ix would you do for suspected Wegener’s granulomatosis?

A

c-ANCA

88
Q

What Ix would you do for suspected Microscopic polyangitis?

A

p-ANCA

89
Q

A 30y/o man presents w/ recurrent GI and nose bleeds. Facial examination shows telangiectasia. What is the diagnosis?

  1. Acromegaly
  2. Cirrhosis
  3. Hereditary haemorrhagic telangiectasia
  4. Peutz-Jegher syndrome
  5. Systemic sclerosis
A

Hereditary haemorrhagic telangiectasia - autosomal dominant condition prone to bleeding. May get haemoptysis.
You would see spider naevi in cirrhosis. Peutz-Jegher syndrome is assoc. w/ dark pigmentation + systemic sclerosis gives you microstomia, tight skin

90
Q

What Ix would you do for adrenal insufficiency?

A

Na+ - low sodium due to excess water from excess ADH due to low cortisol (high cortisol causes decreased ADH)
Short Synacthen test: the cortisol after 30 mins will not have increased much as the adrenal have not responded.

91
Q
Serum prolactin - increased
Testosterone - low
LH - low
FSH - low
What is the most likely Dx?
A

Prolactinoma
Prolactin suppresses gonadotrophins
Increased prolactin causes decreased LH/FSH which causes decreased testosterone therefore secondary hypogonadism

92
Q

What Ix would you do for acromegaly?

A

OGTT: failure of GH suppression with glucose.
Prolactin: increased - prolactinoma or any pituitary tumour (this would compress the stalk which can cause high prolactin) or pregnancy
GH: increased
IGF-1: increased

93
Q

Oestradiol: low
FSH: high
LH: high
What is the most likely diagnosis?

A

Primary ovarian insufficiency
There is decreased negative feedback so increased LH/FSH. Causes of primary ovarian insufficiency - radiotherapy, chemotherapy, AI

94
Q

Low free T4, High TSH + prolactin. What is the likely Dx?

A

Myxoedema (hypothyroidism)
Decreased T4 causes negative feedback which increases TSH + TRH; TRH stimulates prolactin release hence primary hypothyroidism is a cause of mild hyperprolactinaemia.