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Misc > DPD > Flashcards

DPD Flashcards

1
Q

Transudate

What is the protein level and cause?

A

Protein <30g/dL

Caused by heart failure

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2
Q

Exudate

What is the protein level and cause?

A

Protein >30g/dL

Caused by infection or cancer

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3
Q

What are the 2 most common organisms to cause pneumonia?

A
  1. Pneumococcus (Strep pneumoniae)

2. Haemophilus influenzae (this is more common in patients with COPD or smokers)

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4
Q

Pneumococcus (Strep pneumoniae)

Findings on gram staining and microscopy?

A

Gram +ve diplococcus

Stains deep purple

Some pneumococci can autolyse (die) and not take up the stain well

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5
Q

Haemophilus influenzae

Findings on gram staining and microscopy?

A

Gram -ve rod

Stains pink

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6
Q

Treatment for Haemophilus influenzae?

A

Treat with amoxicillin/co-amoxiclav (broad spectrum penicillin with gram -ve cover)

Often tend to give very broad spectrum such as ceftriaxone. But should culture to target therapy.

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7
Q

Treatment for Pneumococcus (Strep pneumoniae)?

A

Treat with benzylpenicillin (may become resistant -higher doses needed)

This is a better choice than a broader agent e.g. tazocin

Often tend to give very broad spectrum such as ceftriaxone. But should culture to target therapy.

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8
Q

Characteristics of gram +ve stain:

Colour?

Wall/membrane structure?

A

Stains purple

Has outer membrane with thick peptidoglycan cell wall (made of N-acetylglucosameine (NAG) and N-acetylmuramic acid (NAM).

PtG wall traps stain

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9
Q

Characteristics of gram -ve stain:

Colour?

Wall/membrane structure?

A

Stains pink

Has inner and outer membranes with thin peptidoglycan cell wall (made of N-acetylglucosameine (NAG) and N-acetylmuramic acid (NAM).

Needs counterstain (safrinin)

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10
Q

Histological findings of TB

A

Multinucleated giant cells surrounding caseating (cheese-like) necrotic centre

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11
Q

What does this histological finding indicate?

Multinucleated giant cells surrounding caseating (cheese-like) necrotic centre

A

TB

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12
Q

What stain is used for Mycobacteria?

A

ZN stain

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13
Q

What is the treatment for TB?

A

4 antibiotics for 2 months, then 2 antibitoics

Isoniazid
Rifampicin
Pyrazinamide
Ethambutol

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14
Q

2 most common causes of adrenocortical failure?

A
  1. Tuberculous Addison’s disease (worldwide)

2. Autoimmune Addison’s disease (UK)

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15
Q

Test for Addison’s

A

Short synACTHen test

Give 250ug synacthen IM
Measure cortisol response

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16
Q

Commonest brain tumour?

A

Metastases from elsewhere

Men= lung cancer
Women= breast cancer
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17
Q

What would you want to look for in someone who has a fit with no other medical history?

A

Hypocalcaemia
Hyponatraemia
Hypoglycaemia
Hypokalcaemia (more often affects heart)

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18
Q

What is the effect of hypokalaemia on the heart?

A

Ventricular fibrillation

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19
Q

What is the effect of hyperkalaemia on the heart?

A

Asystole

Make more and more stable -> asystole

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20
Q

What drug would you administer to someone fitting in A&E if fit doesn’t spontaneously stop?

A

Anti-epileptic
Sedation (medazolam)
May need intubation and ventilation

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21
Q

What BMI range is considered healthy?

Asian range?

A

18.5-24.9

Asian: 18.5-22.9

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22
Q

What BMI range is considered overweight?

A

25-29.9

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23
Q

What BMI range is considered obese?

A

30-34.5 (class 1 obesity)

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24
Q

What is a BMI of 25-29.9 classed as?

A

Overweight

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25
Q

What is a BMI range of 30-34.5 classed as?

A

Class 1 obesity

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26
Q

What is a BMI range of 35-39.5 classed as?

A

Class 2 obesity (severe obesity)

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27
Q

What is a BMI range of 40-50 classed as?

A

Class 3 obesity (morbid obesity)

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28
Q

Features of grade 1 hypertensive retinopathy?

A

Silver wiring

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29
Q

Features of grade 2 hypertensive retinopathy?

A

AV nipping
Narrowing of vein where artery crosses it, and bulges slightly either side of crossing. Means pressure high enough to occlude vein.

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30
Q

Features of grade 3 hypertensive retinopathy?

A

Flame haemorrhages and cotton wool spots (soft exudates)

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31
Q

Features of grade 4 hypertensive retinopathy?

A

Papilloedema (no crisp disc edge)

If there are no other features (flame haemorrhages, cotton wool spots, etc.), suggests brain tumour.

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32
Q

What 3 signs might you find on clinical examination to indicate hypertension?

What feature is also caused by hypertension?

A
  1. Feel a heave
  2. S4 (caused by atria contracting forcefully to overcome an abnormally stiff or hypertrophic ventricle)
  3. Hear bruits

Left ventricular hypertrophy (this is a feature not a sign as can’t be detected on clinical examination unlike left ventricular dilatation)

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33
Q

What is the S4 heart sound in hypertension caused by?

A

Atria contracting forcefully to overcome an abnormally stiff or hypertrophic ventricle

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34
Q

What ophthalmic pathology can prolonged and severe hypertension cause?

A

Hypertensive retinopathy

grades 1-4

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35
Q

What is primary HTN also known as ?

A

Essential HTN

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36
Q

What are secondary causes of HTN?

Hint: 5 main categories

A
  1. Renal disease
    - intrinsic: glomerulonephritis, polyarteritis nodosa, sclerosis, PKD, chronic pyelonephritis

-extrinsic: renal artery stenosis, fibromuscular dysplasia

  1. Endocrine
    - Cushings
    - Conns
    - Pheochromocytoma
    - Acromegaly
    - Hyperparathyroidism
  2. Coarctation of the aorta
  3. Drugs
    - steroids
    - MAO-I
    - Pill
  4. Pregnancy (pre-eclampsia)
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37
Q

What are causes of HTN secondary to renal disease?

A
  • intrinsic: glomerulonephritis, polyarteritis nodosa, sclerosis, PKD, chronic pyelonephritis
  • extrinsic: renal artery stenosis, fibromuscular dysplasia
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38
Q

What are endocrine causes of HTN?

A
  • Cushings
  • Conns
  • Pheochromocytoma
  • Acromegaly
  • Hyperparathyroidism
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39
Q

What drugs can commonly cause HTN?

A
  • Steroids
  • MAO-I
  • Pill
40
Q

What vascular problem can commonly cause HTN?

A

Co-arctation of the aorta

Renal artery stenosis

41
Q

What investigations would you do for HTN?

A 
FBC (polycythaemia)
U+E (K may be low, renal function may be affected)
ECG (LVH)
Urinalysis (nephritis or renal disease)
Fasting glucose (risk of diabetes)
Lipids
Special:
Ca (hyperparathyroidism)
Renin
Aldosterone
24 hr urinary catecholamines
24 hr urinary free cortisol/low dose dexamethasone suppression test
Glucose tolerance test (acromegaly)
Renal US
Imaging of aorta
42
Q

What do these findings suggest?

Renin = 0.4 (1.1-4.5)
Aldosterone= 1600nmol/l (100-450)
24 hr cats normal

A

Conn’s adenoma

Adrenal tumour making lots of aldosterone -> high BP and switching off renin

43
Q

What do these findings suggest?

Renin= 7.4 (1.1-4.5)
Aldos= 900 (100-450)
24 hr cats normal

A

Renal artery stenosis

Reduced pressure in afferent arteriole distal to stenosis, so JGA senses and turns on RAS -> ATII. This constricts efferent arteriole to maintain GFR, and acts on adrenals -> aldosterone.

44
Q

What would you expect the renin and aldosterone levels to be in renal artery stenosis?

A

High renin

High aldosterone

45
Q

What would you expect the renin and aldosterone levels to be in Conn’s?

A

Low renin

High aldosterone

46
Q

Features of pheochromocytoma?

A 
Nervousness
Sweating
Palpitations
Episodic severe HTN (as run out of cats)
Severe vasoconstriction can lead to necrotic bowel
47
Q

What is the management of a pheochromocytoma?

A

(Rehydrate if dehydrated to prevent BP crash)

  1. A-blockade
  2. B-blockade
  3. Localise lesion on US
  4. Surgery

Must give a before b blockers otherwise unopposed stimulation of a receptors leading to vasoconstriction, and a hypertensive crisis (makes BP even higher).

48
Q

What is a MIBG scan?

A

Meta-iodobenzylguanidine scan

Chromaffin-seeking isotope scan that shows up pheochromocytomas and neuroblastomas.

49
Q

What is considered normal BP?

A

SBP: 120-129 and/or
DBP: 80-84

50
Q

What is considered grade 1 HTN?

A

SBP: 140-159 and/or
DBP: 90-99

51
Q

What is the drug treatment algorithm for treating HTN?

A

Step 1:
If under 55 give A
If over 55 or black pt of any age give C or D

Step 2:
A+C or A+D

Step 3:
A+C+D

Step 4:
Add s further diuretic or an a-blocker or a b-blocker

A= ACEi or ARB
C= CCB
D= thiazide-type diuretic
52
Q

What is optimal therapy for HTN?

A
  • intensive lifestyle modification
  • aspirin
  • high dose statin (atorvastatin 40-80mg OD)
  • optimal BP control
  • assessment for probably T2DM

Aggressive management of BP and lipids improves survival

53
Q

How does a PCSK9 inhibitor work and is it useful?

An example?

A

Evolocumab

Stops PCSK9 binding and degrading LDL receptors, so there are more LDL receptors on liver cells so less LDLs in blood adding to risk of CHD.

Very expensive so only for high risk patients (statin resistant and uncontrolled lipids). No impact on mortality and very small absolute risk reduction.

54
Q

What are the symptoms of T2DM?

A

Tiredness/lethargy
Polyuria
Polydipsia

55
Q

How does osmolarity change in T2DM?

A 
Osmolarity increases (430mM)
Glucose slowly rises causing osmotic diuresis causing loss of water. Results in hypernatraemia and hyperglycaemia.
56
Q

Describe the onset of T2DM

A

Insidious

Glucose rises slowly. Often patient only presents once has complication

1/2 of patient’s don’t know they have diabetes.

57
Q

What is the order of microvascular damage in T2DM?

A

Retinopathy -> nephropathy -> neuropathy

58
Q

What are the microvascular complications of T2DM?

What is the aetiology?

A

Retinopathy -> nephropathy -> neuropathy

Caused by glycosylation of basement membrane proteins leading to leaky capillaries.

59
Q

What are the macrovascular complications of T2DM?

What is the aetiology?

A

IHD
CVA (cerebrovasc accident)
Peripheral gangrene

Caused by dyslipidaemia, hypertension, hypercholesterolaemia

60
Q

What are the features of background diabetic retinopathy?

A
  1. Hard exudates (cholesterol)
  2. Blot haemorrhages
  3. Microaneuryms (dots)
61
Q

What is the treatment for background diabetic retinopathy?

A

Improve glucose control

Also inform patient that warning signs are present ad annual retinal screening

62
Q

What are the features of pre-proliferative diabetic retinopathy?

A

Cotton wool spots (soft exudates)

These suggest retinal ischaemia and if left, new vessels will grow. New vessels can then bleed.

63
Q

What is the treatment for pre-proliferative diabetic retinopathy?

A

Pan retinal photocoagulation

Sacrifice 1/3 of peripheral vision

64
Q

What are the features of proliferative diabetic retinopathy?

A

Visible new vessels

These can bleed, and if bleed into vitreous humour, causes blindness as causes fibrosis.

65
Q

What is the treatment for proliferative diabetic retinopathy?

A

Pan retinal photocoagulation

66
Q

What is maculopathy?

A

Hard exudates near macula that threaten direct vision (like background diabetic retinopathy but near macula)

67
Q

Treatment for maculopathy?

A

GRID photocoagulation

68
Q

List long term complications of T2DM

A 
Retinopathy
Nephropathy
Neuropathy
MI
PVD
Stroke/ CVA
Ischaemic foot
Charcot foot
Orthostatic hypotension
Impotence 
Erectile dysfunction
69
Q

Name 2 short acting insulin analogues

A
  1. Lispro (switch of B28 proline to B29 lysine)
  2. Aspart (proline 28 to aspartate 28)

Twice cost of soluble insulin

70
Q

Why does soluble natural insulin have to be injected 30 mins before meals?

A

When given subcutaneously, it forms a hexamer under the skin delaying release. C-peptide is cleaved and A and B chains stick together.

71
Q

Name 2 long acting insulin analogues

A
  1. Glargine (Lantus)
    - Substitution of asparagine to glycine at A21.
    - 2 arginines added at carboxy terminal of B chain (B31, B32 Arg)
  2. Detemir
    - 14 carbon fatty acid chain attached to B29
72
Q

What are the common side effects of:

  1. Metformin?
  2. SU?
  3. Thiazolinediones?
A
  1. Metformin; diarrhoes
  2. SU: occasional reactions
  3. Thiazolinediones: rare hepatic, ?osteoporosis
73
Q

Name GLP-1 analogue examples (incretin)

A

Exenatide (synthetic version of exendin 4 from the Gila monster)

Liraglutide (Victoza, Saxenda)

Semaglutide

74
Q

What is the MOA of incretins?

A
  1. Increase release of endogenous insulin from B cells in pancreas. Along with GIP, leads to increased peripheral glucose uptake.
  2. Reduced release of glucagon from pancreatic a cells to reduce HGO
  3. Reduced gastric emptying
  4. Increased hypothalamic satiety (acts on GLP-1 receptors in hypothalamus)
75
Q

Name examples of DPP4 inhibitors/gliptins

A

Vildagliptin

Sitagliptin

76
Q

What type of drugs are:
Vildagliptin
Sitagliptin

A

DPP4 inhibitors/gliptins

77
Q

What type of drugs are:

Exenatide (synthetic version of exendin 4 from the Gila monster)

Liraglutide (Victoza, Saxenda)

Semaglutide

A

GLP-1 analogues (incretins)

78
Q

Name an SGLT-2 inhibitor

A

Canagliflozin

79
Q

What is Canagliflozin an example of?

A

SGLT-2 inhibitor

80
Q

What is the MOA of SGLT-2 inhibitors (canagliflozin)?

A

Block the SGLT-2 channels that cause 90% of glucose reabsorption from the PCT. They cause glycosuria.

81
Q

What happens to GFR when giving canagliflozin (SGLT2 inhibitor)?

A

Initially reduced but then remains more stable and less steep decline.

Particularly useful in HF as a diuretic

All positive outcomes but concerns over raised amputation risk.

82
Q

What are the 3 histological features of diabetic nephropathy?

A
  1. Glomerular changes
  2. Vascular changes
  3. Tubulointerstitial changes
83
Q

What are the 3 glomerular changes associated with diabetic nephropathy?

A
  1. Mesangial expansion
  2. BM thickening
  3. Glomerulosclerosis
84
Q

CKD increases the risk of cardiovascular events

True or false?

A

True

85
Q

What are the 3 clinical features of diabetic nephropathy?

A
  1. Progressive proteinuria
  2. Increased BP
  3. Deranged renal function
86
Q

What is the normal range of proteinuria?

What is the asymptomatic range?

A

Normal= <30mg/24 hrs

Asymptomatic= 300-3000mg/24 hrs

87
Q

List 4 strategies of intervention for diabetic nephropathy?

A
  1. Diabetes control
  2. BP control
  3. RAS inhibition
  4. Stop smoking
88
Q

Why does an ACEi reduce the GFR?

A

It reduces ATII so there is less constriction of the efferent arteriole, so less pressure in the glomerulus. This reduced GFR (bad) but also reduces albuminuria (good).

89
Q

What should you give all patients with albuminuria?

A

ACEi

90
Q

What condition is an ACEi contradindicated in?

A

Renal artery stenosis

Reduced ATII will lead to almost no pressure in glomerulus, GFR will fall to 0 and become anuric.

91
Q

What are possible complications of anuria?

A
  • hyperkalaemia
  • pulmonary oedema
  • acidosis
92
Q

What are the implications of renal failure?

A
  • electrolyte misbalance (hyperkal, hyponat)
  • acidosis
  • fluid retention
  • waste product retention
  • secretory failure (erythropoietin, 1,25 vit D) -> anaemia and renal bone disease
93
Q

What are the symptoms of renal failure?

A
  • tiredness
  • SOB, oedema
  • pruritis, nocturia, feeling cold, twitching
  • poor appetite, nausea, weight loss
  • anaemia
  • renal bone disease
94
Q

What are the options for renal replacement therapy?

A
  1. dialysis (HD or PD)
  2. transplantation

or
conservative care

95
Q

What is supportive care and what are the key aims?

A

Care that helps the patient and family to cope with the condition and it’s treatment.

Aims:

  • communication with patient and family
  • awareness of patient being near end of life
  • advance planning of care
  • appropriate active interventions

Misc (2 decks)

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