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6th Year Endo/Haem/Misc MJ > dpd > Flashcards

dpd Flashcards

1
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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2
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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3
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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4
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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5
Q

what confirms coeliac dis dx + what will be seen

A

Duodenal biopsy

Villous atrophy, crypt hyperplasia

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6
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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7
Q

tx for coeliac disease

A

Strict, lifelong gluten-free diet

Vit D supplements for vit D deficiency

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8
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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9
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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10
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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11
Q

what is mx of AF that is <48h onset

A

DC cardioversion to revert back to SR or chemical cardioversion with flecainide

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12
Q

what is mx of AF that is >48h onset

A

Anticoagulate w/ LMWH + rate control with BB/digoxin

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

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13
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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14
Q

What does Trousseau’s sign indicate?

A

HIGH CALCIUM / hypercalcaemia
-carpopedal spasm with BP cuff on
OR
sign of thrombophlebitis in pancreatic C

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15
Q

virchows node indicates what

A

supraclavicular LN indicates gastric cancer

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16
Q

troisiers sign indicates what

A

enlargement of left supraclavicular LN due to secondary involvement

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17
Q

grey turners sign indicates what

A

bruising on flanks associated with pancreatitis (retroperitoneal haemorrhage)

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18
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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19
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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20
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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21
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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22
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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23
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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24
Q

How does Haemolytic Uraemic Syndrome present?

A

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

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25
Q

What is Thrombotic Thrombocytopenic Purpura (TTP)?

A

HUS + Fever + neuro complications eg confusion, seizures

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26
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:
-Autoimmune e.g. SLE
-drugs
-infection
-MAHA

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27
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) - SB

- Haustra is a feature of large bowel - Haustra go Halfway

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28
Q

What is the Tx for small bowel obstruction?

A

NBM

Drip + suck (IV fluids, NGT)

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29
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 (normal = 40-200) ; 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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30
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

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31
Q

What single Ix best indicates hypovolaemia?

A 
Urine sodium (normal = 40-200)
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)

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32
Q

classification of hyponatraemia

A

hypovolaemia
euvolaemia
hypervolaemia

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33
Q

causes, pres, + tx of HYPOvolaemia

A

Causes: D, V, diuretics, salt losing nephropathy

Pres: Postural hypotension, tachycardia, reduced skin turgor, dry mucous membranes

Low urine Na+ (must measure off diuretics)
Ks will reabsorb more Na+

Tx: Fluids 0.9% saline

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34
Q

causes, Ix + tx of Euvolaemia

A

causes: ENDOCRINE - SIADH, Hypothyroidism, Adrenal Insufficiency

Ix: TFTs; short synacthen test (normal: increased cortisol).

Low plasma osmolality due to decreased Na+.
Increased plasma osmolality due to increased SIADH

Tx: Fluid restriction

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35
Q

What are the causes + presentation of hypervolaemia?

A

Cause: FAILURES - cardiac failure, cirrhosis, nephrotic syndrome

Presentation: Signs of fluid OVERLOAD e.g. peripheral oedema, increased JVP

Low urine Na+ (due to reduced bloodflow to kidney - increased renin + Angiotensin - increased aldosterone - increased Na + reabsoprtion.)

36
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

37
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
38
Q

what is mx 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 MYELINOLYSIS
  • If fitting or decreased GCS - 3% HYPERTONIC SALINE
39
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

40
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

41
Q

What are the microvascular complications of diabetes?

A

Think eyes, kidneys, feet

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

42
Q

What are the macrovascular complications of diabetes?

A

Think heart, brain, vessels

MI
Stroke
Peripheral vascular disease

43
Q

what are metabolic complications of diabetes

A

DKA
HHS
Hypoglycaemia

44
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

45
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

LVH

  • 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
46
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

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

47
Q

what renal stones on XR are semi-opaque vs radio-lucent

A

cystine stones: semi-opaque

urate + xanthine stones: radio-lucent

48
Q

What are the DDx of loin pain w/ haematuria?

A

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

49
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.
50
Q

What does a high Ca2+ and high PTH indicate?

A

Hyperparathyroidism

51
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)

52
Q

Where is ALP made?

A

Liver and Bone (osteoblasts)

53
Q

What does an increased ALP indicate?

A

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

54
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 monoclonal Ig or Ig fragment in serum +/or urine
-usu assoc with osteolytic bone disease, anaemia and renal failure

55
Q

Ix for MM

A

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

56
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

57
Q

What does a cavitating lesion on a CXR indicate?

A

III + malignancy

INF - S. aureus, TB, Klebsiella in alcoholics
INFLAMM - 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

58
Q

what does interstitial shadowing indicate on CXR

A

fluid or pus eg HF

59
Q

how does pleural effusion present on CXR

A

homogenous white

60
Q

what does bilateral hilar lymphadenopathy indicate

A

sarcoidosis

61
Q

what are ddx for pulmonary cavitating lesion

A

=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 PE
  • 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
62
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 HF therefore ankle oedema likely to be due to low albumin.
63
Q

what is nephrotic syndrome

A
  • Proteinuria, Oedema + Hypoalbuminaemia
  • Due to increased permeability of GBM to protein
  • Other features include: prone to TE dis e.g. renal vein thrombosis because they lose endogenous anticoagulants in urine
64
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

65
Q

What is membranous glomerulonephritis?

A

Non-proliferative glomerulonephritis

  • Thickening of glomerular BM 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 deposits. SPIKES + DOME seen on SILVER stain

66
Q

what is minimal change GN

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

67
Q

What is the Ix for minimal change glomerulonephritis?

A
  • Electron microscopy shows effacement of podocyte foot processes
  • Light microscopy is NORMAL
  • Immunoflorescence - negative as not due to immune complex
68
Q

What is focal segmental glomerulosclerosis (FSGS)?

A

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

69
Q

how can FSGS present

A

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

70
Q

How can focal segmental glomerulosclerosis be diagnosed?

A

focal sclerosis

71
Q

What is IgA nephropathy?

A 
Proliferative glomerulopathy (nephritic syndrome) which often presents as asymptomatic non-visible haematuria within DAYS of an INFECTION
- Increased BP + proteinuria.
72
Q

What is the Ix for IgA nephropathy?

A

Renal biopsy: IgA deposition in mesangium

73
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.

74
Q

What is post-streptococcal glomerulonephritis?

A

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

75
Q

What is the Ix for post-streptococcal glomerulonephritis?

A

Increased anti-streptococcal Ab titre

Increased anti-DNAse B

76
Q

What is membranoproliferative glomerulonephritis?

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

77
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
78
Q

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

A

c-ANCA

79
Q

What Ix would you do for suspected Microscopic polyangitis?

A

p-ANCA

80
Q

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

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

Hereditary haemorrhagic telangiectasia - ADom 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

81
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.

82
Q

Serum prolactin - increased
Testosterone - low

LH - low
FSH - low
What is the most likely Dx?

A

prolactinoma

prolactin supresses gonadotrophins

83
Q

What Ix would you do for acromegaly?

A

IGF-1 testing
OGTT - fail to supress GH with glucose
Prolactin - incr - prolactinoma or any pituitary tumour (compress stalk) or pregnancy

84
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

85
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.

6th Year Endo/Haem/Misc MJ (7 decks)

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