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mccqe 1 > Medicine > Flashcards

Medicine Flashcards

1
Q

Grading scale for murmurs

A

Levine scale
1 slightest possible murmur heard by trained ear
2 soft murmur heard when in optimal condition
3 moderately loud. no thrill
4 loud and associated with a palpable thrill
5 loud with thrill. heard with stethoscope lightly touching chest
6 loud, thrill heard with stethoscope not touching skin

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2
Q

Guilliain- Barre syndrome is most likely associated with which organism

A

Campylobacter jejune

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3
Q

Guilliain-barre symptoms are caused by..

A

loss of myelin

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4
Q

GBS definition

A

acute rapidly evolving demyelinating inflammatory polyradiculoneuropathy that often starts
in the distal lower limbs and ascends

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5
Q

signs and symptoms of GBS

A

■ sensory: distal and symmetric paresthesias, loss of proprioception and vibration sense, neuropathic
pain
■ motor: weakness starting distally in legs, areflexia
■ autonomic: blood pressure dysregulation, arrhythmias, bladder dysfunction

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6
Q

investigation for GBS

A

■ CSF: albuminocytologic dissociation (high protein, normal WBC)
■ EMG/NCS: conduction block, differential or focal (motor > sensory) slowing, decreased F-wave,
sural sparing

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7
Q

subtypes of GBS

A

• subtypes

  1. acute inflammatory demyelinating polyneuropathy (AIDP)
  2. acute motor-sensory axonal neuropathy (AMSAN)
  3. acute motor axonal neuropathy (AMAN)
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8
Q

treatments of GBS

A

• treatment

■ IVIG or plasmapheresis, ± pain management, monitor vitals and vital capacity

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9
Q

antidote for nerve gas poisoning

A

atropine

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10
Q

Diabetic retinopathy - clinical features

A

Non proliferative
pre proliferative
proliferative

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11
Q

leading cause of blindness

A

diabetic retinopathy

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12
Q

prevention of diabetic retinopathy

A

Tight glycemic control

Annual visits to optometrist or ophthalmologist

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13
Q

what is diabetic retinopathy

A

a microvascular complication of poorly controlled diabetes.

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14
Q

treatment of diabetic retinopathy

A

Pan-retinal and focal retinal laser
photocoagulation reduces the risk of visual loss
in patients with macular edema.
intravitreal injection of corticosteroid or anti-VEGF for foveal involved diabetic macular edema

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15
Q

how does loss of vision occur in diabetic retinopathy

A

loss of vision due to
■ progressive microangiopathy leading to macular edema
■ progressive DR → neovascularization → traction → RD and vitreous hemorrhage
■ rubeosis iridis (neovascularization of the iris) leading to neovascular glaucoma (poor prognosis)
■ macular ischemia

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16
Q

non- proliferative diabetic retinopathy

A

increased vascular permeability and retinal ischemia
■ microaneurysms
■ dot and blot hemorrhages
■ hard exudates (lipid deposits), non-specific for DR
■ macular edema

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17
Q

pre-proliferative diabetic retinopathy

A

■ non-proliferative findings plus:
◆ venous beading (in ≥2 of 4 retinal quadrants)
◆ intraretinal microvascular anomalies (IRMA) in 1 of 4 retinal quadrants
– IRMA: dilated, leaky vessels within the retina
◆ cotton wool spots (nerve fibre layer infarcts)

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18
Q

proliferative diabetic retinopathy

A

■ 5% of patients with DM will reach this stage
■ neovascularization of iris, disc, retina to vitreous
◆ neovascularization of iris (rubeosis iridis) can lead to neovascular glaucoma
◆ vitreous hemorrhage, bleeding from fragile new vessels, fibrous tissue can contract causing
tractional RD
■ high risk of severe vision loss secondary to vitreous hemorrhage, RD
soft exudates indicate ischaemia

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19
Q

extra ocular muscle palsy associated with diabetic retinopathy

A
  • usually CN III infarct
  • pupil usually spared in diabetic CN III palsy, but ptosis is observed
  • may involve CN IV and VI
  • usually recover within few months
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20
Q

peripheral neuropathy facts

A
  • as proprioception reduces it becomes more difficult to walk on uneven surfaces
  • many patients are injured yearly by putting their feet on radiators or sitting to close to the fire.
  • specific footwear to protect feet
  • foot shape changes due to glycosylation of collagen
  • charcot Joint
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21
Q

microvascular complications of diabetes

A

Neuropathy, retinopathy, nephropathy, glaucoma and cataracts

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22
Q

microvascular complications of diabetes

A

coronary artery disease, Stroke, peripheral vascular disease (and therefore ulcers and gangrene)

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23
Q

other complications of diabetes

A 
increased risk of infections
pregnancy complications
metabolic difficulties
impotence
autonomic neuropathy
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24
Q

causes of sudden loss of vision in diabetic patients

A

central retinal artery occlusion
retinal detachment
vitreous haemorrhage

25
Q

eye assessments for diabetic patients include

A

opthalmoscopy through dilated pupils
retinal photography
fluorecein angiography
slit lamp examination

26
Q

what is peripheral neuropathy

A

a symmetrical sensory polyneuropathy, initially affecting distal lower extremities.
decreased or loss of ankle reflexes occurs early in disease.
progressive loss increases the risk of ulcer formation

27
Q

large fibre loss - peripheral neuropathy

A

loss of vibration

loss of proprioception

28
Q

Small fiber loss peripheral neuropathy

A

loss of light touch
loss of temperature
impairment of pain

29
Q

drugs approved by Health Canada for peripheral neuropathy

A

duloxetine

pregabalin

30
Q

Dengue fever

A

Common Arboviral infection

31
Q

clinical incubation period dengue fever

A

5-10 days

32
Q

vector for dengue fever including breeding areas

A

Aedes aegypti mosquito which prefers to breed in clean water and common in urban areas with higher incidences in the Welter months

33
Q

symptoms of dengue fever

A

lethargy
biphasic fever (present for 2 days which resolves and is then followed by a second fever)
headache - especially retro orbital pain
arthralgia
myalgia
rash - usually with second fever. maculopapular starting on trunk and spreading to limbs

34
Q

Severe cases/complications of Dengue

A

Dengue shock syndrome
Dengue haemorrhage fever
these have immunological basis - if previous immunity to dengue serotypes –> increases risk

35
Q

dengue antibodies

A

IgG usually remains positive for life

antibodies do not give protection against dengue as more than one serotype but is not at increased risk of complication

36
Q

pre renal causes of AKI

A

Drugs
Hypercalcaemia
Hypovolaemia (absolute and effect)

37
Q

Drugs causing AKI

A

ACE/ARB
NSAIDS
cyclosporin
Tacrolimus

38
Q

diagnosing Zollinger -Ellison syndrome

A

fasting serum gastrin level

39
Q

Anti-Saccharomyces cerevisiae antibodies

A

A group of antibodies directed at components of the cell wall of the yeast Saccharomyces cerevisiae. Associated with chronic inflammatory bowel disease (particularly Crohn disease).

40
Q

Schilling test

A

A test to determine the cause of B12 deficiency. Patients ingest radiolabelled B12 and then its urinary excretion is measured. Excretion will be normal if the cause is a dietary deficiency. If excretion is low (suggesting malabsorption), the test is repeated with orally administered intrinsic factor (IF). If excretion normalizes, the cause is IF deficiency. If excretion still remains low, the test is repeated with antibiotics, and then pancreatic enzymes to rule out bacterial overgrowth and pancreatic insufficiency, respectively.

41
Q

p-ANCA

A

An autoantibody against myeloperoxidase granules (present in the perinuclear region of cytoplasm). p-ANCA levels are increased in patients with ulcerative colitis, autoimmune systemic vasculitis (especially Churg-Strauss syndrome and microscopic polyangiitis) and primary sclerosing cholangitis.

42
Q

fecal lactoferrin

A

A marker of intestinal inflammation used to assess for, e.g., inflammatory bowel disease (IBD)

43
Q

Whipple disease

A

An infectious disease caused by the bacteria Tropheryma whipplei. It is notoriously difficult to diagnose because of its variable presentation. Findings often include chronic malabsorptive diarrhea, weight loss, migratory non-deforming arthritis, lymphadenopathy, and a low-grade fever.

44
Q

Tropical Sprue

A

A bacterial infection that is associated with a stay in the tropics or subtropics and leads to structural damage of the intestinal mucosa. Characterized by chronic diarrhea with subsequent malabsorption, abdominal cramps, progressive weight loss, and fatigue.

45
Q

Hepatitis C

A

A viral infection that causes acute or chronic inflammation of the liver after an incubation period of 2 weeks to 6 months. Usually transmitted parenterally but can be transmitted sexually or perinatally. Inflammation is usually mild or not present at all and resolves within a few weeks or months. Can rarely cause acute liver failure. Often leads to chronic hepatitis.

46
Q

test to confirm acute hepatitis A

A

Anti-HAV IgM

47
Q

primary sclerosing cholangitis

A

Primary sclerosing cholangitis (PSC) is a progressive chronic inflammation of both the intrahepatic and extrahepatic bile ducts. While the exact etiology is unknown, there is a strong association with autoimmune diseases, particularly ulcerative colitis (UC). In the early stages, PSC is usually asymptomatic. Later in the course of the disease, patients present with symptoms of cholestasis (e.g., pruritus, jaundice). Laboratory abnormalities include elevated liver function tests and autoantibodies (pANCA in up to 80% of cases). Magnetic resonance cholangiopancreatography (MRCP) or endoscopic retrograde cholangiopancreatography (ERCP) is performed to confirm the diagnosis. Management is primarily symptomatic, with liver transplantation reserved for end-stage liver disease.

48
Q

hydatid cyst disease

A

A helminthic infection caused by cestodes of the genus Echinococcus (e.g., E. granulosus, E. multilocularis). Infection is typically acquired by accidental ingestion of Echinococcus eggs, which are shed in the feces of infected dogs. Infection results in cystic lesions in the liver (75% of cases), lung (15% of cases), and, rarely, other organs.

49
Q

albendazole

A

An orally administered, broad-spectrum antihelminthic drug that is used to treat echinococcosis, cysticercosis, pinworm infection (enterobiasis), hookworm infection (ancylostomiasis, necatoriasis), ascariasis, trichuriasis, and strongyloidiasis. Mechanism of action: inhibition of microtubule synthesis.

50
Q

HBsAg

A

Surface antigen
Protein on the surface of HBV; first evidence of infection
Anti‑HBs
Indicates immunity to HBV due to vaccination or resolved infection
Usually appears 1–3 months after infection.

51
Q

HBcAg

A

Core antigen
Protein of the nucleocapsid
Anti‑HBc
Anti-HBC IgM indicates recent infection with HBV (≤ 6 months)
Anti-HBc IgG indicates resolved or chronic infections

52
Q

HBeAg

A

Envelope antigen
Protein secreted by the virus that indicates viral replication and infectivity
Anti‑HBe
Indicates long-term clearance of HBV

53
Q

Hepatitis A virus (HAV)

A 
Picornavirus
Non-enveloped virus
Positive sense, single-stranded, linear RNA
Fecal-oral
15–50
Acute hepatitis: fever, malaise, loss of appetite, nausea, abdominal pain, jaundice, ↑ AST/ALT
Children < 6 years often have no symptoms
Anti-HAV IgM
Supportive
Food and water hygiene
Immunization
Full recovery within ∼ 3 months
Does not become chronic
54
Q

IE - staphylococcus aureus

A

Most common cause of acute IE for all groups (including IV drug users and patients with prosthetic valves or pacemakers/ICDs)
Affects previously healthy valves
Usually fatal within 6 weeks (if left untreated)

55
Q

IE - Viridans streptococci

A

Most common cause of subacute IE, especially in predamaged native valves (mainly the mitral valve) and in prosthetic valves (≥ 60 days after surgery)
Common cause of IE following dental procedures
Produce dextrans that facilitate binding fibrin-platelet aggregates on damaged heart valves

56
Q

IE - Viridans streptococci

A

Most common cause of subacute IE, especially in predamaged native valves (mainly the mitral valve) and in prosthetic valves (≥ 60 days after surgery)
Common cause of IE following dental procedures
Produce dextrans that facilitate binding fibrin-platelet aggregates on damaged heart valves

57
Q

Risk factors for chronic venous disease

A

Higher age and female sex (see “Epidemiology” above)
Family history of venous disease
Ligamentous laxity
Sedentary lifestyle and prolonged standing
Obesity
Pregnancy
Smoking
Prior thrombosis (postthrombotic syndrome)
Prior extremity trauma
Congenital abnormalities

58
Q

primary prevention rheumatic fever

A

prompt antibiotic treatment (e.g., penicillin V) of GAS tonsillopharyngitis diagnosed by throat culture or rapid strep test

59
Q

secondary prevention rheumatic fever

A

Antibiotic prophylaxis to prevent recurrence
Drug of choice: IM penicillin G benzathine
In patients with a penicillin allergy: oral macrolides
Usually administered every 28 days
Immediately follows antibiotic treatment of acute rheumatic fever (see “Treatment” above)
Duration depends on risk and severity of original episode
Rheumatic fever without carditis: 5 years or until the patient is age 21 (whichever is longer)
Rheumatic fever with carditis: 10 years or until the patient is age 21 (whichever is longer)
Rheumatic fever with carditis and permanent valvular heart defects: 10 years or until age 40 (whichever is longer)

mccqe 1 (8 decks)

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