RACP 2023 rapid fire Flashcards

1
Q

Describe the roles of the phrenic nerve and its location

A
  • C3-C5 nerve roots
  • motor - diaphragm innervation
  • sensory - central diaphragm, pericardium, central pleura
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2
Q

Name the 4 phases of Hep B infection

A

tolerance -> clearance -> control -> escape

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3
Q

In the tolerance phase of chronic Hep B, what is the management approach?

A

Monitor every 6-12 months

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4
Q

Why should treatment be considered in the immune phase of chronic Hep B?

A
  • high HBV DNA, High HBe Ag, abnormal LFTs
  • RISK of progression to cirrhosis & HCC
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5
Q

Describe the immune control (phase 3) of chronic Hep B

A
  • Anti-Hbe, Hbe-Ag NEG
  • HBV DNA low
  • monitor - observe 6-12 months
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6
Q

Describe the features of immune escape in chronic HBV

A
  • Anti-Hbe, Hbe-Ag - low
  • HBV DNA HIGH
  • normal LFTs
  • TREAT as risk of progression to HCC and fibrosis
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7
Q

When should a pregnancy patient be treated with Hep B?

A
  • If the viral load is >200,000
  • re-check bloods 26-28 weeks and commence treatment 3rd trimester; treat with TDF monotherapy
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8
Q

When assessing the phase of chronic B infection, what are the key blood tests?

A
  • HBV-DNA
  • HbeAg, Anti-HbeAg
  • liver panel
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9
Q

What would be required at birth for a baby with a Hep B +ve mother, regardless of HBV DNA level?

A

Hep B vaccination
Hep B IG

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10
Q

True or false. Breast feeding is a risk for Hep B transmission

A

False

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11
Q

A mother wants to have a vaginal delivery. what is the implication if she has Hep B

A
  • should be guided by levels* (for decision for treatment with procedures that confer risk, levels guide this)
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12
Q

What is the clinical significance of Hepatitis E with respect to population

A
  • rapid progression to fulminant liver failure
  • particular high risk groups = pregnant women, solid transplant recipients, pre-exisitng chronic liver disease
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13
Q

95% of non-occlusive bowel ischaemic occur in the watershed areas. What are these?

A

splenic flexute, rectosigmoid junciton

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14
Q

Name two common alpha 2 agonists and antagonists

A
  • angonists - dexmedtomadine, methyldopa, clonodine
  • antagonists - some 2nd gen antipyschotics e.g. quetiapine, risperadone
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15
Q

Name two common alpha 1 antagonists and agonists

A
  • agonists = metaraminol, midodrine
  • antagonists = tamsulosin (selective), prazocin
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16
Q

Name one b1 antagonist and agonist that is commonly used

A

b1 agonist = dobutamine
b1 antagonist = all your beta blockers really

17
Q

What is the role of the beta 2 receptor

A
  • smooth muscle vasodilation
18
Q

Type 1 (distal) and Type 2 (proximal) RTA have common associated causes. What are these?

A
  1. Type 1 distal
    - autoimmune causes - SLE, Sjogrens, SSc, PBC, lithium, NSAIDs, MM, paracetamol overdose

Type 2 proximal
- most common MM, TENOFOVIR

19
Q

What is the most common cause of hyporenic hypoaldosteronism?

A

diabetic nephropathy-destruction of JG apparatus due to vascular hyalinosis

20
Q

Describe the pathophys of type 1 RTA

A
  • affects the distal tubule
  • causes by damage to intercalated cells
  • unable to SECRETE HYDROGEN (cant produce bicarb and therefore get it reabsorbed)
  • low bicarb, low K (as trying to reduce serum acidosis)
  • basic urine pH>5.5
21
Q

Describe the pathophys of type 2 proximal RTA

A
  • DECREASED ability to reabsorb bicarb
  • urine pH>7, will reduce to <5.5 if bicarb is low (when serum bicarb is low, some reabsorbtion takes place)
  • hypokalemia, low bicarb
  • test by giving bicarb and seeing if pH>7.5 and bicarb excretion >15%
22
Q

Explain the pathohys of Type 4 ETA

A

aldosterone deficiency or resistance
- unable to secrete K or H = hyperK
- reduced excretion of NH4+ (main buffer for acid base balance)
- LOW urine pH
*often caused by hyporenemic hypoaldosteronisim

23
Q

What is the mechanism of type 4 RTA if a patient has diabetes?

A

Hyporeninemic hypoaldosteronism: most common cause in adults is diabetic nephropathy-destruction of JG apparatus due to vascular hyalinosis

24
Q

A cell contains many important structures. What is the role of the following - ribosome, rough ER, smooth ER, golgi, lysosome?

A
  • ribosome - protein production
  • rough ER - protein folding
  • smooth ER - hormone/lipid synthesis
  • golgi - protein transport
  • lysosome - recyling + apoptosis
25
What is the inheritance pattern of Haemophilia?
X-linked recessive
26
What factor range would cause a patient to present with bleeding ONLY after major trauma or surgery?
5-40%
27
What factor level in haemophilia would trigger spontaneously bleeding?
<1%
28
What is the hallmark feature of haemophilia in severe disease?
The hallmark clinical presentation of both hemophilia A and B is joint (hemarthroses) and muscle bleeding, which typically presents in severe disease.
29
List two key differences between haemophilia and vWBD
1. haemophilia - x linked recessive - MSK bleeding 2. vWBD - mucocutaneous bleeding more likely - males + females affected equally
30
What are the two main arms to treatment in haemophilia?
- factor replacement therapy - prophylaxis -> Emicizumab - factor IX and X (replaces factor VIIIa) -> Concizumab - mAb against tissue factor pathway inhibitor (used in Haem B with factor IX inhibitors)