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Finals > Renal, Urogenital, Endocrine > Flashcards

Renal, Urogenital, Endocrine Flashcards

1
Q

What are the criteria to diagnose an AKI?

A

Rise in creatinine of >25 micromol/L in 48 hours
Rise in creatinine of >50% in 7 days
Urine output <0.5ml/kg/hr for >6 hours

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2
Q

Risk factors for AKI?

A

CKD
HF
T2DM
Liver disease
>65 years
Cognitive impairment
Nephrotoxic medications e.g. NSAIDS, ACEi
Contrast in CT

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3
Q

Three generic causes of AKI?

A

Pre renal
Renal
Post renal

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4
Q

Pre renal causes of AKI?

A

Most common cause
Due to inadequate blood supply
Can be due to:
Dehydration
Hypotension/ shock
Heart failure

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5
Q

What are some renal causes of AKI?

A

Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis

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6
Q

Post renal causes of AKI?

A

Due to obstruction of outflow

Kidney stones
Masses in abdomen or pelvis e.g cancer
Ureter strictures
Enlarged prostate e.g cancer or BPH

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7
Q

Investigations for AKI?

A

Urinalysis

Leucocytes—> ?infection
Nitrites —>?infection
Protein —> ?acute nephritis
Blood —> ?acute nephritis
Glucose —> ?diabetes

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8
Q

Potential consequences of AKI?

A

Hyperkalaemia
Fluid overload, heart failure, pulmonary oedema
Metabolic acidosis
Uraemia (high urea) —> encephalopathy or pericarditis

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9
Q

Causes of CKD?

A

Diabetes
Hypertension
Age related decline
Glomerulonephritis
Pyelonephritis
PKD
Medications e.g. NSAIDS, PPIs and lithium

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10
Q

How is CKD diagnosed?

A

eGFR- two tests required 3 months apart
Proteinuria… Urine albumin:creatinine ratio >3mg/mmol significant

Diagnosis requires an eGFR <60 and/or proteinuria in both tests 3 months apart.

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11
Q

Stages of kidney function?

A

G score based on eGFR
G1- eGFR >90
G2 - 60-89
G3a 45-59
G3b 30-44
G4 15-29
G5 <15 - end stage renal failure

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12
Q

What stage of CKD would an eGFR with…
89
17
61
37

A

89 —> G2
17 —> G4
61 —> G2
37 —> G3b

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13
Q

What eGFR is required to diagnose CKD

A

eGFR <60
(Or proteinuria)

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14
Q

Management of CKD?

A

Slow progression of disease
Reduce risk of CVD
Treating complications

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15
Q

Features of ADPKD?

A

Autosomal dominant polycystic kidney disease

Hypertension
Recurrent UTIs
Flank pain
Haematuria
Palpable kidneys
Renal impairment
Renal stones

Extra Renal manifestations
- Liver cysts- 70% can cause hepatomegaly
- Berry aneurysms- 8% can rupture and cause SAH
- CVD: mitral valve prolapse, aortic dissection, mitral/tricuspid incompetence, aortic root dilation
- cysts in other organs e.g. pancreas, spleen,

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16
Q

2nd line for stress incontinence?

A

Duloxetine
If 1st line pelvic floor, reduction in caffeine and alcohol tried and not for surgery

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17
Q

Urge incontinence management?

A

1st- Bladder retraining
2nd- bladder stabilising drugs e.g. oxybutinin, tolterodine or darifenacin (immediate release oxybutinin should be avoided in frail older women)
- mirabegron, a beta 3 agonist- if concerned about anti-cholinergic SEs in frail old ladies

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18
Q

What are the two pharmacological management options for stress and urge incontinence?

A

Stress- duloxetine
Urge- oxybutinin (urge-oxy, both begin with vowels)

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19
Q

Hypertension and hypokalaemia and lethargy. Likely cause?

A

Primary hyperaldosteronism

Can be caused by bilateral idiopathic adrenal hyperplasia- 70%
Adrenal adenoma secreting aldosterone- Conn’s syndrome

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20
Q

First line investigation for primary hyperaldosteroneism?

A

Serum aldosterone/renin ratio

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21
Q

Patient presents with acute renal failure and haemoptysis, what are the two most likely causes?

A

Goodpasture syndrome- associated with anti-GBM antibodies
Granulomatisis with polyangitis aka Wegeners granulomatosis- vascularised associated with ANCA antibodies

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22
Q

Patient with haemoptysis, deranged electrolytes, raised creatinine, reduced urine output, a wheeze, sinusitis and a saddle shaped nose. What’s going on?

A

Wegeners granulomatosis aka granulomatosis with polyamgitis

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23
Q

How are most types of Glomerulonephritis treated?

A

Immunosuppression ie steroids
Blood pressure control through ACEi or ARBs

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24
Q

23yo man presents with dark urine, reduced urine output, some ankle swelling, had a cold 2-3 weeks ago but otherwise no PMH. What’s going on?

A

Signs of nephritic syndrome- haematuria, oligourea, fluid retention, AND proteinurea
Likely: post streptococcal Glomerulonephritis

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25
Q

What is nephritic syndrome?

A

Nephritic syndrome/nephritis describes a group of symptoms, not a disease
Has features of (but these aren’t a criteria to be classed as nephritic sx)
Haematuria
Oliguria
Proteinuria- less than 3g/24hrs- more will be NEPHROTIC syndrome
Fluid retention

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26
Q

What is nephrotic syndrome?

A

Group of sx without specific cause. But have a criteria to be classed as nephrotic sx (unlike nephritic sx)
Criteria
- peripheral oedema
- PROTEINUREA >3g/24hours
- serum albumin under 25g/L
- hypercholesterolaemia

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27
Q

Signs of CKD?

A

Usually asymptomatic until stage 4 (eGFR 15-29) but can have:
- pruritis- itching
- loss of appetite
- nausea
- oedema
- muscle cramps
- perioheral neuropathy
- pallor
- hypertension

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28
Q

What is required to diagnose CKD?

A

eGFR < 60
OR
proteinuria

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29
Q

How is proteinuria measured, what result is significant?

A

Urine albumin : creatinine ratio
Significant >3 mg/mmol

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30
Q

What is the G score and the A score?

A

G score is the eGFR score
A score is based on the albumin:creatinine ratio

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31
Q

High calcium, high PTH. What type of hyperparathyroidism is this? Cause?

A

Primary
Parathyroid gland tumour

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32
Q

What causes secondary hyperparathyroidism? Would Ca and PTH be raised or low?

A

CKD
Low vit D

Ca would be low
PTH would be raised

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33
Q

What causes tertiary parathyroidosm?

A

Result of long term secondary. Parathyroid gland undergoes hyperplasia to maintain the high release of PTH. If cause is treated, still releases high PTH

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34
Q

Management of tertiary hyperparathyroidism?

A

Surgical resection of hyperplased area

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35
Q

3 actions of PTH

A

To raise calcium by:
Increases gut reabsorption of calcium
Increased reabsorption of calcium and phosphate from the kidney
Increased osteoclast activity to release calcium and phosphate from bones

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36
Q

AKI complications

A

Hyperkalaemia
Haemorrhage
Pulmonary oedema

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37
Q

What’s released into the blood when rhabdomyalysis occurs?

A

Creatinine kinase
Myoglobin

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38
Q

How can rhabdomyolysis cause an AKI?

A

Myoglobin released filter through the glomerulus and precipitate, obstructing the tubules

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39
Q

What common drugs should be stopped if someone has an AKI?

A

NSAIDs
ACEi
Metformin
Furosemide

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40
Q

Management of AKI caused by rhabdomyolysis?

A

IV fluid rehydration

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41
Q

Acute renal failure and suspecting an intrinsic renal cause, other than the usual blood workup, what blood tests would you want?

A

ANCA- ?Wegeners granulomatosis
anti-GBM- ?Goodpastures?

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42
Q

Define nephrotic syndrome

A

Proteinuria >3g/24hours
Hypoalbuminaemia <30g/L
Oedema

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43
Q

Most common cause of nephrotic syndrome in children, adults and elderly?
Other causes?

A

Children- minimal change disease
Adults- membranous nephropathy
Elderly- focal segmental glomerulosclerosis

Other causes
- diabetes
- amyloidosis
- SLE
- drugs

44
Q

Complications of nephrotic syndrome?

A

Increased susceptibility to infections- lose immunoglobulins in urine and tx is immunosuppressive e.g. steroids
Increased risk of VTE- loss of clotting factors in urine and increased fibrinogen
Hyperlipidaemia- increased synthesis of lipoproteins in liver due to hypoalbunaemia

45
Q

What do you do to determine cause in hypovolaemic hyponatraemia?

A

Measure urinary sodium- indicates if sodium is lost renally or extra-renally
Renally if urinary Na >20
Extra-Renally if Na<20

46
Q

Hypovolaemic hyponatraemia renal loss causes?

A

Addisons disease
Diuretics
Diuretic phase of renal failure

47
Q

Hypovolaemic hyponatraemia extra-renal loss causes?

A

Diarrhoea
Vomiting
Burns
Fistula

48
Q

Euvolaemic hyponatraemia what investigation to determine cause?

A

Urine osmolality
If low (<500mmol/kg)- ?hypothyroidism, ?psychogenic polydipsia
If high (>500mmol/kg)- SIADH

49
Q

What changes occur to the urine in SIADH? What type of hyponatraemia is caused by SIADH?

A

High urine osmolality/ high urine sodium

Euvolaemic hyponatraemia- the increased ADH causes blood dilution and reduced Na but not enough to cause a fluid overload

50
Q

Are the following intracellular or extracellular?
- sodium
- potassium

A

Sodium is extracellular- hence the higher (compared to K) conc in blood
Potassium is intracellular

51
Q

How do you calculate serum osmolality?

A

(2x Na) + glucose + urea
Sometimes include K in the (2x Na+K)
All in mmol/L

52
Q

How do you test for adrenal insufficiency?

A

Short synacthen test

53
Q

When correcting hyponatraemia, how quickly should you aim to correct the Na deficit?

A

Less than 10mmol/l per 24 hours

54
Q

What happens if severe hyponatraemia is corrected too quickly?

A

Severe is below 120 mmol/l

Central pontine myelinolysis

55
Q

What’s a normal osmolality of serum and urine?

A

Plasma- 275-295 mOsm/kg
Urine- around 100

56
Q

A patient presents with dysuria and urinary frequency, what are you looking for on urine dipstick to confirm the diagnosis?

A

Nitrites- suggest bacteria present as they break down nitrates into nitrites
Leukocyte esterase- indicates leukocyte level (ie WBCs)- raised indicates infection

Nitrites are better indication of a UTI.
If both present, treat as UTI
If only nitrites- treat as UTI
If only leukocytes raised- don’t treat unless clinical evidence of UTI

If only one raised, send to microbiology

57
Q

How does aldosterone act on the body?

A

Aldosterone is a mineralocorticoid steroid hormone

Acts on kidney

Causes/increases:
Na reabsorption from distal tubule
K secretion from distal tubule —> can get hypokalaemia
H secretion from collecting ducts

58
Q

What would you expect to see in the ix of choice in primary hyperaldosteronism?

A

High aldosterone and low renin

59
Q

What would you expect to see in the ix of choice in secondary hyperaldosteronism?

A

High aldosterone and high renin

60
Q

Most common cause of secondary hypertension?

A

Hyperaldosteroneism

61
Q

Cause and pathophysiology of primary hyperaldosteronism?

A

Adrenal glands directly produce too much aldosterone

Causes- most common
- b/l adrenal hyperplasia
- an adrenal adenoma secreting aldosterone- aka Conn’s syndrome

Serum renin will be low as negative feedback causes it to decrease

62
Q

Causes and pathophysiology of secondary hyperaldosteronism?

A

Secondary so overstimulated from elsewhere!

Excess renin stimulating adrenal gland to release aldosterone

Causes
- renal artery stenosis
- renal artery obstruction
- HF

63
Q

What is diabetes insipidus?

A

A condition where either secretion or response to ADH is impaired.
I.e. decreased secretion or an insensitivity to it

64
Q

Features of diabetes insipidus?

A

Polyuria
Polydipsia
Hypernatraemia

65
Q

Investigations for diabetes insipidus?

A

High plasma osmolality with low urine osmolality
- a urine osmolality >700 mOsm/kg excludes diabetes insipidus

Water deprivation test

66
Q

What test can exclude diabetes insipidus?

A

If urine osmolality is above 700
As DI leads to a high plasma osmolality and a low urine osmolality

67
Q

What are the two types of diabetes insipidus?

A

Cranial or nephrogenic

Cranial is where not enough ADH is produced by the hypothalamus
Nephrogenic is where the kidneys don’t respond to ADH

68
Q

What is the water deprivation test? What is it aka?
How does it work?

A

Aka: desmopressin stimulation test

Tests for diabetes insipidus

Method
- avoid fluids for 8 hours- fluid deprivation
- urine osmolality is measured
- synthetic ADH (desmopressin) is given
- 8 hours later urine osmolality is measured again

In cranial DI, the urine osmolality will go from low to high as the kidneys are able to respond to the desmopressin
So, in nephrogenic DI, urine osmolality will be low and stay low

69
Q

Desmopressin test. What will the urine osmolality after desmopressin deprivation and after desmopressin administration in….
- cranial DI
- nephrogenic DI
- primary polydipsia

A

Desmopressin is synthetic ADH

Cranial DI
- after deprivation- low (as not enough ADH to reabsorption water)
- after ADH- high- as kidneys respond

Nephrogenic DI
- after deprivation- low
- after ADH- stays low as kidneys can’t respond

Primary polydipsia
- urine osmolality is high after deprivation of water as there is no ADH problem and the body is not still secreted water when dehydrated. This is caused by excessive drinking

70
Q

How do you calculate the anion gap?

A

(Na + K) - (Bicarb + Cl)

71
Q

Normal anion gap

A

~3-12 mmol/L
Every source says something slightly different in range of 3 to 18

72
Q

From the history, how would you differentiate between IgA nephropathy and post streptococcal glomerulonephritis?

A

PSGN usually develops 1-2weeks post strep infection e.g. sore throat
IgA is usually 1-2 days after URTI

They both usually present with haematuria

73
Q

What bedside test can be done to differentiate between AKI and CKD?

A

Renal USS
Usually, CKD can lead to small kidneys.
Exceptions- PKD and early stages of diabetic nephropathy where they can increase in size before later shrinking

74
Q

Management of IgA nephropathy

A

If isolated event with proteinuria <500 and normal eGFR- only follow up to check renal function

If persistent proteinuria >500- ACEi

If eGFR is falling and not responding to ACEi- immunosuppression with corticosteroids

75
Q

What blood test can be done to confirm recent streptococcal infection?

A

Raised anti-streptolysin O titre
Low C3

76
Q

Management of nephrogenic and cranial diabetes insipidus?

A

Cranial- synthetic ADH (desmopressin)
Nephrogenic- thiazide like diuretics and low salt/protein diet +/- NSAIDS

77
Q

What is a pheochromocytoma?

A

A tumour of chromaffin cells in the adrenal medulla of adrenal glands
So, secretes unregulated amounts of adrenaline

78
Q

How does a pheeochromocytoma usually present?

A

Bursts of a excessive sympathetic activity,
Adrenaline is released in bursts from the phaeochromocytoma

79
Q

How do you diagnose/ investigate for a phaeochromocytoma?

A

24 hour catecholamines
Plasma free metanephrines

*metanephrines are breakdown products if adrenaline with a linger half life so have less dramatic fluctuations. 24 hour catecholamines are done do see the wider picture too

80
Q

Symptoms and signs of a phaeochromocytoma?

A

Fluctuating symptoms of increased sympathetic activity
- anxiety
- sweating
- headache
- hypertension
- palpitations, tachycardia
And ‘paroxysmal AF’

81
Q

Management of a phaeochromocytoma?

A

Alpha blockers e.g. phenoxybenzamine
Beta blockers once established on alpha blockers
Adrenalectomy- to remove tumour. Should be medically managed pre surgery to reduce anaesthetic and surgical risk

82
Q

What medication can be given to patients with PKD and their disease is progressing rapidly or they’re in stage 2 or 3 CKD?

A

Tolvaptan- a vasopressin receptor 2 antagonist

83
Q

Investigation for acromegaly?

A

Serum IGF-1 levels (insulin-like growth factor) is 1st line

OGTT is used to confirm with lack of GH suppression when given glucose

84
Q

What is sick euthyroid syndrome?

A

In acute illness can occur
T3 and T4 are low and TSH doesn’t increase in response to this
Usually resolves with treatment of cause

85
Q

For a patient who is newly diagnosed with T2DM and has a PMH of angina, what treatment should they be prescribed?

A

Metformin- titrated up as tolerated
Once metformin is established, start an SGLT-2 inhibitor (e.g. dapaglifozin) due to CVD disease (used as organ protection rather than glycemic control)
Should be given in addition to metformin in patients with:
- high risk of CVD, QRISK >10%
- established CVD e.g. angina
- chronic HF

86
Q

Diabetes sick day rules?

A

If a diabetic becomes unwell

  • Increase frequency of glucose monitoring to at least 4 hourly
  • at least 3L of fluids /day
  • if can’t eat, drink sugary drinks
  • continue normal drugs- including insulin, to prevent DKA
87
Q

How does Addisons disease usually present?

A

Reduced cortisol and aldosterone produced from adrenal glands

Lethargy, weakness, anorexia, n&v, weight loss, salt-craving
Hyperpigmentation of palmar creases
Vitiligo- loss of skin pigment
Loss of oubic hair in women
Hypotension
Hypoglycaemia
Hyponatraemia and hyperkalaemia
Severe: collapse, shock, pyrexia

88
Q

What is addisons disease?

A

A for Adrenal
Addisons is primary hypoadrenalism. Ie the adrenal glands aren’t functioning properly
This leads to low cortisol and aldosterone

89
Q

T2DM diagnostic criteria?

A

Either plasma glucose or HBA1c

If symptomatic
- fasting glucose >7 mmol/l
- random glucose >11.1 mmol/l
*if asymptomatic, these must be repeated to diagnose

HBA1c >48 (6.5%) mmol/mol

90
Q

Which diabetic drugs are higher risk of causing hypoglycaemia?

A

Insulin
Sulfonylureas e.g. gliclazide

91
Q

What electrolyte abnormalities do you often see in Conn’s syndrome?

A

Hypokalaemia
Hypernatraemia (or higher in normal range)—> hypertension

Conn’s is specifically an adrenal adenoma that secreted excess aldosterone. The most common cause of hyperaldosteronism is now recognised as bilateral hyperplasia of adrenal glands

Conns is caused by increased aldosterone release from adrenal glands —> causes Na reabsorption and K and H secretion in kidneys. Can also get alkalosis due to loss of H

92
Q

What vision abnormality can be seen in acromegaly?

A

Bitemporal hemianopia- due to compression of optic chiasm from pituitary adenoma

93
Q

How would you test for a phaeochromocytoma?

A

Plasma metanephrines OR 24 hour urine catecholamines

94
Q

What is Conn’s syndrome?

A

Conn’ syndrome- an adrenal adenoma secreting excessive aldosterone ( causing a Primary hyperaldosteroneism)

95
Q

What is Cushing’s disease?
What is Cushing’s syndrome?

A

Cushing’s syndrome reflects the clinical picture of prolonged elevation of cortisol.
Cushing’s disease is the specific condition where a pituitary adenoma secretes excess ACTH which leads to Cushing’s syndrome

96
Q

Brief overview of the adrenal axis?

A

Hypothalamus releases CRH in response to low cortisol
CRH stimulates anterior pituitary to release ACTH
ACTH stimulates adrenal glands to release cortisol
Cortisol is a steroid hormone that:
- suppresses the immune system
- inhibits bone formation
- raises blood glucose
- increases metabolism
- increases alertness

97
Q

What does CRH and ACTH stand for?

A

CRH- Corticotrophin Releasing Hormone
ACTH- Adrenocorticotrophic hormone

98
Q

What medications are aldosterone antagonists?

A

Eplerenone
Spironolactone

99
Q

What medication can be used if hyponatraemia in SIADH is not alone corrected by fluid restriction?

A

Vaptans e.g. Tolvaptan
- they’re ADH receptor blockers

100
Q

T2DM diagnosis
Plasma glucose for
- fasting
- random
- OGTT

HbA1c

A

Fasting > 7 mmol/l
Random > 11 mmol/l
OGTT- give 75g glucose drink, 2 hours later >11 mmol/l

HbA1c > 48 mmol/mol (>42 is prediabetes)

101
Q

Sweating, increased alertness, tremour, always hot with neck stiffness, recent illness, what is it?

A

Hyperthyroidism
De quervains thyroidistis- post illness, usually resolves

102
Q

What is hydroxychloroquine used to treat and what do patients need to be monitored for?

A

SLE- discoid and systemic
Rheumatoid arthritis

Eye function as higher risk of severe retinopathy. Visual acuity testing every 6-12 months (standard reading chart)

Can be used in pregnancy

103
Q

Incubation period for gonorrhoea and chlamydia?

A

Gonorrhoea 2-5 days
Chlamydia 7-21 days but often asymptomatic

104
Q

19yo male with dysuria and penile discharge, key differentiating question to differentiate between chlamydia and gonorrhoea?

A

When did they have unprotected sex
Both present with dysuria and penile discharge but chlamydia presents 7-21 days after unprotected sex, gonorrhoea is 2-5 days

105
Q

Gonorrhoea tx?

A

IM ceftriaxone 1g (used to also give Azithromycin, not anymore)

106
Q

Management of chlamydia

A

Doxycycline 7 days
Used to be Azithromycin. Azithromycin still used 2nd line and in pregnancy(or erythromycin or amoxicillin)

Finals (13 decks)

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