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Year 3 > Metabolic > Flashcards

Metabolic Flashcards

1
Q

Gold standard imaging for renal cell carcinoma (RCC)

A

= CT imaging of abdominal-pelvis pre- and post- IV contrast

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2
Q

Most common type of adult renal tumour?

A

= renal cell carcinoma (RCC)

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3
Q

The following microscopic findings in a renal biopsy indicates what?

  • polyhedral clear cells
  • dark staining nuclei
    cytoplasm rich with lipid + glycogen granules
A

= renal cell carcinoma (RCC)

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4
Q

Classic triad of RCC

A
  • haematuria
  • mass
  • flank pain
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5
Q

Treatment for RCC

A
  • surgical removal (nephrectomy) combined,
  • immunotherapy (INF-a, or IL-2 agents)
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6
Q

Biological agents which may be used in treatment of RCC?

A

= tyrosine kinase inhibitors

(e.g., Sunitinub, Pazopanib)

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7
Q

Majority of prostate cancers arise from which zone:

  • transitional zone
  • central zone
  • peripheral zone
A
  • peripheral zone
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8
Q

2 types of prostate adenocarcinomas

A
  • acinar adenocarcinoma
  • ductal adenocarcinoma
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9
Q

Most common type of prostate adenocarcinoma?

  • acinar adenocarcinoma
  • ductal adenocarcinoma
A
  • acinar adenocarcinoma
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10
Q

Which of the following prostate adenocarcinoma grows + metastasises faster?

  • acinar adenocarcinoma
  • ductal adenocarcinoma
A
  • ductal adenocarcinoma
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11
Q

Investigations for prostate cancer (3)

A
  • PSA levels
  • DRE
  • multi-parametric MRI scan
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12
Q

Scan used to diagnose prostate cancer

A

= multi-parametric MRI scan (mp-MRI)

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13
Q

2 types of biopsy techniques for diagnosing prostate cancer

A
  • transperineal biopsy
  • transrectal ultrasound guided (TRUS) biopsy
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14
Q

Which of the following types of biopsy is most commonly used in diagnosing prostate cancer?

  • transperineal biopsy
  • transrectal ultrasound-guided (TRUS) biopsy
A
  • transperineal biopsy

(reduced risk of infection)

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15
Q

Which scoring system is used to grade prostatic cancers based on their histological appearance?

A

= Gleason Grading System

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16
Q

How is the Gleason Grading Score calculated?

A

= calculated as sum of most common growth pattern + second most common growth pattern seen

(higher the score, worse the prognosis)

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17
Q

Management of prostate cancer is related to risk stratification. What is used to calculate this? (3)

A
  • PSA levels
  • Gleason score
  • T staging (TNM)
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18
Q

What is brachytherapy?

(in relation to prostate cancer)

A

= internal radiaiton, transperineal implantation of radioactive seeds into prostate gland

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19
Q

Mainstay treatment options from localised or locally advanced prostate cancer? (2)

A
  • surgical management (radical prostatectomy)
  • radiotherapy (external-beam or brachytherapy)
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20
Q

Treatment effectively used in metastatic prostate cancer?

A

= anti-androgen therapy

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21
Q

Orchidectomy

A

= surgical removal of one or both testicles

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22
Q

Which of the following types of primary testicular tumours are more common:

  • germ cell tumour (GCT)
  • non-germ cell tumour (NGCTs)
A
  • germ cell tumour (GCT)
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23
Q

Seminomas + non-seminomatous tumours are subtypes of which of the following primary testicular tumours?

  • germ cell tumour (GCT)
  • non-germ cell tumour (NGCTs)
A
  • germ cell tumour (GCT)
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24
Q

Which of the following type of primary testicular tumours tend to be benign?

  • germ cell tumour (GCT)
  • non-germ cell tumour (NGCTs)
A
  • non-germ cell tumour (NGCTs)
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25
Q

Which of the following sub-types of GCT testicular tumours have a better prognosis?

  • seminomas
  • non-seminomatous GCTs
A
  • seminomas
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26
Q

Which type of imaging is used for initial assessment of scrotal lumps?

A

= scrotal USS

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27
Q

What is used to diagnose testicular cancer? (2)

A
  • imaging (USS)
  • tumour markers
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28
Q

Most common type of renal stone?

A

= calcium oxalate

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29
Q

Which of the following are often larger, softer renal stones, most common cause of “staghorn calculi”?

  • struvite stones
  • urate stones
  • cystine stones
A
  • struvite stones
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30
Q

Which of the following type of renal stone forms in alkaline urine?

  • struvite stones
  • magnesium ammonium phosphate stones
  • urate stones
  • cystine stones
A
  • struvite stones
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31
Q

Which of the following type of renal stone forms in people with high purine diets?

  • struvite stones
  • magnesium ammonium phosphate stones
  • urate stones
  • cystine stones
A
  • urate stones
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32
Q

Gold standard imaging for renal stones?

A

= non-contrast CT scan of renal tract (KUB)

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33
Q

Treatment of renal calculi

A

Most stones will pass spontaneously with:
- fluid resuscitation
- analgesia

Other management options:
- extracorporeal shock wave lithotripsy (ESWL)
- percutaneous nephrolithotomy (PCNL)
- flexible uretero-renoscopy (URS)

If signs of infection or AKI, urgent decompression required by:
- stent insertion, or
- nephrostomy

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34
Q

Which of the following type of renal stone is associated with a familial disorder (genetic testing advised)

  • struvite stones
  • magnesium ammonium phosphate stones
  • urate stones
  • cystine stones
A
  • cystine stones
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35
Q

Stage 1 AKI is classified as

A

Creatinine, 1.5-1.9x the baseline

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36
Q

Stage 2 AKI is classified as

A

Creatinine, 2-2.9x the baseline

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37
Q

Stage 3 AKI is classified as

A

Creatinine, >3x the baseline

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38
Q

Pre-renal causes of AKI

A

(hypovolaemia or reduced amount of blood)

  • sepsis
  • dehydration
  • haemorrhage
  • cardiac failure
  • liver failure
  • renal artery stenosis
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39
Q

Intra-renal causes of AKI

A
  • nephrotoxins/ drugs: NSAIDs, ACEi or ARBs, antibiotics (aminoglycosides), chemotherapy (cisplatin)
  • parenchymal disease: glomerulonephritis, acute tubulointerstitial nephritis, rhabdomyolysis, haemolytic uraemia syndrome (HUS), multiple myeloma
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40
Q

Post-renal causes of AKI

A

(obstruction)

Ureteric - retroperitoneal fibrosis, bilateral renal stones, tumours (mural or extra-mural)
Bladder - acute urinary retention, blocked catheter
Urethral - prostatic enlargement (BPH or malignancy), renal stones

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41
Q

High urine specific gravity + osmolarity, as well as low Na excretion is indicative of which type of cause of an AKI?

  • pre-renal
  • intra-renal
    -post-renal
A
  • pre-renal
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42
Q

Drugs which should be potentially stopped in AKI? (4)

A
  • ACEi or ARBs
  • NSAIDs
  • Aminoglycoside antibiotics
  • Potassium-sparing diuretics (risk of hyperkalaemia)
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43
Q

eGFR range in G1 CKD

A

> 90 mL/min/1.73m^2

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44
Q

eGFR range in G2 CKD

A

60-89 mL/min/1.73m^2

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45
Q

eGFR range in G3a CKA

A

45-59 mL/min/1.73m^2

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46
Q

eGFR range in G3b CKD

A

30-44 mL/min/1.73m^2

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47
Q

eGFR range in G4 CKD

A

15-29 mL/min/1.73m^2

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48
Q

eGFR range in G5 CKD

A

<15 mL/min/1.73m^2

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49
Q

2 most common causes of CKD

A
  • diabetes
  • vascular disease
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50
Q

In CKD, what happens to:
- serum creatinine
- eGFR
- albumin:creatinine ratio

A
  • serum creatinine - high
  • eGFR - reduces
  • albumin:creatinine ratio increases
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51
Q

How do you diagnose CKD?

(1-2, 3-5)

A

CKD stages 1-2: requires additional evidence of renal disease (other then eGFR), such as:
- proteinuria
- urine sediment abnormalities
- electrolyte abnormalities
- structural abnormalities
- histological abnormalities
- history of kidney transplantation

CKD stages 3-5: can be diagnosed based on eGFR alone

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52
Q

How often are CKD patients monitored if they are considered low-moderate risk?

A

= annually

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53
Q

How often are CKD patients monitored if they are considered high risk?

A

= every 6 months

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54
Q

How often are CKD patients monitored if they are considered very high risk?

A

= every 3-4 months

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55
Q

What value of eGFR indicates dialysis?

A

= 5-10 ml/min/1.73m^2

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56
Q

2 types of dialysis

A
  • haemodialysis
  • peritoneal dialysis
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57
Q

Complications of CKD

A

Mnemonic ‘A WET BED’

Acid-base balance – metabolic acidosis
Water removal – pulmonary oedema
Erythropoiesis – anaemic of chronic kidney disease
Toxin removal – uraemic encephalopathy
BP control – CVD
Electrolyte balance – hyperkalaemia
vitamin D activation – bone-mineral disorder of chronic kidney disease (CKD-BMD), previously referred to as renal osteodystrophy

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58
Q

Which of the following is preferred when gaining access for dialysis? why?

  • arterio-venous fistula
  • tunnelled central venous catheter
A
  • arterio-venous fistula

(less complications e.g., infection)

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59
Q

What is pyelonephritis?

A

= inflammation of kidney parenchyma + renal pelvis due to bacterial infection

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60
Q

What is the most common causative organism in pyelonephritis?

A

= E. coli

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61
Q

Classic triad of pyelonephritis presentation

A
  • fever
  • unilateral loin pain (rarely bilateral)
  • nausea + vomiting
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62
Q

What is important to rule out in a patient presenting with loin pain in suspected pyelonephritis?

A

= AAA rupture

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63
Q

Investigations for pyelonephritis

A

Urinalysis - assess for nitrates + leucocytes
Urine culture
Routine bloods
Renal USS scan - to check for any evidence of an obstruction

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64
Q

Which scan is used to check for obstruction in a patient with suspected pyelonephritis?

And if evidence of an obstruction is found, what scan should be performed after?

A

= renal USS

= non-contrast CT (CT KUB)

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65
Q

Treatment for pyelonephritis

A
  • appropriate resuscitation if needed
  • start empirical antibiotics (against anticipated causative organism(
  • IV fluids if appropriate, suitable analgesia, + anti-emetics
  • tailor antibiotic therapy once sensitivities are available

(consider admission in those cases where pt is clinically unstable, significantly dehydrates, or with co-morbidities)

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66
Q

Which of the following is the insulin regimen of choice for patients with T1DM:

  • basal-bolus regime
  • 1,2,3 injections per day
  • continuous insulin infusion via pump
A
  • basal-bolus regime
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67
Q

Which of the following of the following basal-bolus regimes are first-line?

  • twice‑daily insulin detemir
  • once-daily insulin glargine
A
  • twice‑daily insulin detemir
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68
Q

What is serum C-peptide a measure of?

A

= insulin production

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69
Q

Is serum C-peptide usually high or low in T1DM?

A

= low

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70
Q

What autoantibodies are associated with T1DM? (3)

A
  • anti-islet cell antibodies
  • anti GAD antibodies
  • anti-insulin antibodies
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71
Q

Diagnostic criteria for T1DM

A

If symptomatic:
- fasting glucose >/= 7.0 mmol/L
- random glucose >/= 11.1 mmol/L

If asymptomatic above needs to be demonstrated twice

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72
Q

BMI > 25 is classed as?

A

= overweight or obese

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73
Q

What conditions make up metabolic syndrome? (4)

A
  • hypertension
  • hyperglycaemia
  • excess fat around waist
  • hypercholesterolaemia
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74
Q

Obesity Class I BMI range

A

30-34.9 kg/m2

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75
Q

Obesity Class II BMI range

A

35-39.9 kg/m2

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76
Q

Obesity Class III BMI range

A

> /= 40 kg/m2

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77
Q

How does Orlistat work?

A

= prevents absorption of dietary fat

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78
Q

How does Liraglutide work in weight loss?

A

= delaying gastric emptying + inducing early satiety (satisfaction) resulting in overall reducing in calorie intake + weight loss

79
Q

What is dumping syndrome?

A

= group of symptoms caused by food rapidly emptying or being ‘dumped’ from the stomach into the small intestine. This results in undigested food in the small intestine that the body finds hard to absorb

Symptoms: sweating, bloating, abdominal cramps/ pain, diarrhoea + nausea

80
Q

What can be used to treat hyperthyroidism SYMPTOMS?

A

= beta-blocker (Propanolol)

81
Q

First-line definitive treatment in Graves’ disease?

A

= radioactive iodine

82
Q

What is first-line definitive treatment in Graves’ disease if radioactive iodine + surgery are unsuitable?

A

= anti-thyroid drugs (e.g., Carbimazole)

83
Q

In relation to using anti-thyroid drugs in hyperthyroidism, what is a ‘block + replace regimen’, compared to a ‘titration regimen’?

A

Block + replace - involves using a higher dose of Carbimazole which blocks all production, and then using Levothyroxine to replace

Titration regime - Carbimazole titrated to maintain normal levels

84
Q

Most common cause of hyperthyroidism in developed countries?

A

= Graves’ disease

85
Q

What is Graves’ disease?

A

= autoimmune condition resulting in overproduction of thyroid hormones, due to formation of antibodies to thyroid-stimulating hormone (TSH) receptors

86
Q

What exceptions are there to using radioactive iodine first-line in treating Graves’ disease? (4)

A
  • pregnancy
  • attempts to conceive within next 4-6 months
  • presence of active eye disease
  • concerns about compression or malignancy
87
Q

What would you expect TSH, fT3 + fT4 values to be in a patient with Graves’ disease?

A

TSH - low
fT3 - high
fT4 - high

88
Q

Which antibodies are present in Graves’ disease?

A

= TSH-receptor antibodies

89
Q

What is Plummer’s disease AKA?

A

= toxic multi nodular goitre

90
Q

What type of scan is used to help diagnose a toxic multi nodular goitre?

A

= radioisotope scan (I-123 - preferred isotope)

91
Q

What are the 2 management options for treating multi nodular goitre? (and which is first-line)?

A
  • surgery (thyroidectomy)
  • radioactive iodine < first-line
92
Q

Most common cause of hypothyroidism in the developed world?

A

= Hashimoto’s thyroiditis (AKA autoimmune thyroiditis)

93
Q

Management in hypothyroidism?

A

= Levothyroxine

94
Q

In pregnancy would should be done to Levothyroxine dose?

A

= increased, due to increased demands during pregnancy

95
Q

DKA is characterised by what 3 things?

A
  • hyperglycaemia
  • ketosis
  • metabolic acidosis
96
Q

What pH indicates DKA?

A

= < 7.3

97
Q

Is DKA more common complication in type 1 or type 2 diabetes?

A

= type 1

98
Q

Drug: -flozin’

A

= SLGLT-2 inhibitor

99
Q

What is the first-line drug choice in T2DM treatment?

A

= Metformin

100
Q

Which type of diabetes has a stronger genetic predisposition?

A

= type 2 DM

101
Q

What HbA1c value is diagnostic of diabetes?

A

> /= 48 mmol/mol

102
Q

On treatment, what is the HbA1c threshold which indicates diabetes is not well controlled?

A

> 58 mmol/mol

103
Q

What drug is added to T2DM treatment if patient is at risk of developing CVD, or has CVD or chronic HF?

A

= SLGT-2 inhibitor

104
Q

T2DM: If triple therapy is not effective what kind of rug can be added and swapped for another patient is currently on?

A

= GLP-1 mimetic

105
Q

What is Addison’s disease?

A

= also known as primary adrenal insufficiency, refers specifically to when the adrenal glands have been damaged, resulting in reduced cortisol + aldosterone

106
Q

Most common cause of adrenal insufficiency?

A

= autoimmune

107
Q

What is secondary adrenal insufficiency?

A

= results from inadequate adrenocorticotropic hormone (ACTH), this is a result of loss or damage to the pituitary gland

108
Q

What is tertiary adrenal insufficiency?

A

= results from inadequate corticotropin-releasing hormone (CRH) release by the hypothalamus

109
Q

What is tertiary adrenal insufficiency usually caused by?

A

= patients taking long-term oral steroids > leads to suppression of the hypothalamus

110
Q

Electrolyte imbalances associated with Addison’s disease (sodium, potassium, glucose + calcium)

A
  • hyponatraemia
  • hyperkalaemia
  • hypoglycaemia
  • hypercalcaemia
111
Q

Test of choice for diagnosing adrenal insufficiency

A

= short Synacthen test

112
Q

How does the short Synacthen test work?

A

Involves giving a dose of Synacthen (synthetic ACTH). Blood cortisol checked before, 30, and 60 minutes after dose

Failure of cortisol to increase indicates either:
- primary adrenal insufficiency
- very significant adrenal atrophy, after prolonged absence of ACTH in secondary adrenal insufficiency

113
Q

When differentiating between primary adrenal insufficiency + adrenal atrophy due to secondary adrenal insufficiency, how will ACTH levels differ?

A

Primary - ACTH high
Secondary - ACTH low

114
Q

Treatment in adrenal insufficiency, including what is used to replace cortisol + aldosterone

A

= replacement steroids

Hydrocortisone - used to replace cortisol
Fludrocortisone - used to replace aldosterone

115
Q

Adrenal insufficiency: What should be done to steroid dose in acute illness?

A

= double it

116
Q

What is given to patient with adrenal crisis?

A

IM or IV hydrocortisone
IV fluids
IV dextrose (correct hypoglycaemia)

117
Q

What is Cushing’s disease?

A

= refers to pituitary adenoma secreting excessive adrenocorticotropic hormone (ACTH), stimulating excessive cortisol release from the adrenal glands

118
Q

What is paraneoplastic Cushing’s syndrome?

A

= occurs when ATCH is released from a tumour somewhere other than the pituitary gland (ectopic ACTH)

119
Q

Most common cause of paraneoplastic Cushing’s syndrome?

A

= small cell carcinoma

120
Q

What does skin pigmentation tell you about the cause of Cushing’s syndrome?

A

If present - indicates high ACTH > so either caused by Cushing’s disease or ectopic ACTH

(can exclude adrenal adenoma or exogenous steroids)

121
Q

1st-line test for Cushing’s syndrome?

A

= overnight dexamethasone suppression test

122
Q

Which test can be used to identify determine the cause of Cushing’s syndrome?

A

= High-dose 48 hour dexamethasone suppression test

123
Q

In a low-dose dexamethasone suppression test, what would the following different causes of Cushing’s syndrome cortisol result be?

  • normal
  • adrenal adenoma
  • pituitary adenoma
  • ectopic ACTH
A

Normal - low
Adrenal adenoma - not suppressed
Pituitary adenoma - not suppressed
Ectopic ACTH - not suppressed

124
Q

In a high-dose dexamethasone suppression test, what would the following different causes of Cushing’s syndrome cortisol result be?

  • normal
  • adrenal adenoma
  • pituitary adenoma
  • ectopic ACTH
A
  • normal - low
  • adrenal adenoma - not suppressed
  • pituitary adenoma - low
  • ectopic ACTH - not suppressed
125
Q

Primary treatment option for Cushing’s disease?

A

= trans-sphenoidal removal or pituitary adenoma

126
Q

What is Conn’s syndrome?

A

= refers to an adrenal adenoma producing too much aldosterone (type of primary hyperaldosteronism)

127
Q

In primary hyperaldosteronism, would you expect renin levels to be high or low?

A

= low

128
Q

In secondary hyperaldosteronism, would you expect renin levels to be high or low?

A

high

129
Q

What is secondary hyperaldosteronism caused by?

A

= caused by excessive renin stimulating release of excessive aldosterone

130
Q

Why might excess renin be released in secondary hyperaldosteronism? (3)

A
  • Renal artery stenosis
  • HF
  • Liver cirrhosis + ascites
131
Q

First investigation in suspected hyperaldosteronism?

A

= aldosteron-to-renin ratio (ARR)

132
Q

A high-aldosterone to low renin ratio is seen in which of the following:

  • primary hyperaldosteronism
  • secondary hyperaldosteronism
A
  • primary hyperaldosteronism
133
Q

A high-aldosterone to high renin ratio is seen in which of the following:

  • primary hyperaldosteronism
  • secondary hyperaldosteronism
A
  • secondary hyperaldosteronism
134
Q

Is hyperaldosteronism patients can present with which of the following:

  • metabolic acidosis
  • metabolic alkalosis
A
  • metabolic alkalosis

(loss of hydrogen ions in the urine occurs when excess aldosterone (Conn’s syndrome) increases the activity of a sodium-hydrogen exchange protein in the kidney. This increases the retention of sodium ions whilst pumping hydrogen ions into the renal tubule)

135
Q

Medical treatment for hyperaldosteronism?

A

= aldosterone antagonists (e.g., Eplerenone or Spironolactone)

136
Q

What is a phaeochromocytoma?

A

= = tumour of the adrenal glands that secretes unregulated + excessive amounts of catecholamines (adrenaline)

137
Q

What cells produce adrenaline?

A

= chromaffin cells

138
Q

First-line investigation for suspected phaeochromocytoma?

A

= 24 hr urine metanephrines

(metanephrine - breakdown product of adrenaline)

139
Q

Management of phaeochromocytoma (3)

A
  • alpha-blockers
  • beta-blocker
  • surgical removal of tumour
140
Q

What is acromegaly?

A

= disorder that occurs when your body makes too much growth hormone (GH)

141
Q

What is acromegaly most commonly caused by?

A

= pituitary adenoma

142
Q

What visual defect is seen in patients with acromegaly?

A

= intemporal hemianopia

143
Q

First-line test for acromegaly?

A

= serum IFG-1 levels

144
Q

First-line treatment in acromegaly?

A

= trans-sphenoidal surgery, to remove pituitary tumour

145
Q

Drugs which block the release of growth hormone (2)

A
  • somatostatin analogues
  • dopamine agonists
146
Q

What causes primary hyperparathyroidism?

A

= tumour of the parathyroid

147
Q

What causes secondary hyperparathyroidism?

A

= low vitamin D or CKD

148
Q

What causes tertiary hyperparathyroidism?

A

= hyperplasia of parathyroid gland

(happens when secondary hyperparathyroidism continues for extended periods of time, after being treated

Hyperplasia of parathyroid glands > produce more parathyroid > when secondary cause treated, baseline parathyroid hormone remains high > hypercalcaemia)

149
Q

What 3 ways does parathyroid hormone act to raise blood calcium?

A
  • increasing osteoclast activity in bone
  • increasing calcium reabsorption in kidneys
  • increased vitamin D activity – resulting in increased calcium absorption in intestines
150
Q

Symptoms of hypercalcaemia?

A

‘Stones, bones, groans and psychiatric groans’

  • kidney stones
  • painful bones
  • abdominal groans (constipation, nausea + vomiting)
  • psychiatric moans (fatigue, depression + psychosis)
151
Q

What is SIADH?

A

= refers to the increased release of ADH from the posterior pituitary. This increases water reabsorption from urine, diluting blood > leads to hyponatraemia

152
Q

In SIADH, what do you expect urine osmolality + urinary sodium to be?

A

Urinary osmolarity: high
Urinary sodium: high

153
Q

3 important causes of SIADH to remember (there are many)

A
  • small cell lung cancer
  • post-operative
  • SSRIs
154
Q

Investigations for SIADH

A
  • Urine osmolarity
  • Urine sodium concentration
155
Q

What is the effect of Demeclocycline, in the treatment of ADH?

A

= reduces responsiveness of collecting tubule cells to ADH

156
Q

Where does osmotic demyelination syndrome, AKA central pontine myelinosis (CPM) arise from?

A

= is a complication of long-term severe hyponatraemia being treated too quickly

157
Q

First-line treatment for steroid-induced diabetes?

A

= Sulfonylureas

158
Q

Which of the following works most immediate to lower blood sugar?

  • DDP-4 inhibitor
  • Pioglitazone
  • Sulfonylurea
  • SGLT-2 inhibitor
A
  • Sulfonylurea
158
Q

Which of the following works to lower blood sugar by causing the kidneys to remove sugar from the body through the urine?

  • DDP-4 inhibitor
  • Pioglitazone
  • Sulfonylurea
  • SGLT-2 inhibitor
A
  • SGLT-2 inhibitor
159
Q

Which DDP-4 inhibitor can be used to lower blood sugar in patient with kidney disease?

A

= linagliptin

160
Q

Which metabolic imbalance is seen in Cushing’s disease?

  • hypokalaemic metabolic alkalosis
  • hyperkalaemic metabolic acidosis
  • hyperkalaemic metabolic alkalosis
  • hypokalaemic metabolic acidosis
A
  • hypokalaemic metabolic alkalosis
161
Q

Most common type of glomerulonephritis?

A

= IgA Nephropathy (Berger’s disease)

162
Q

Symptoms associated with nephritic syndrome (4)

A
  • haematuria
  • oliguria
  • proteinuria
  • fluid retention
163
Q

Nephrotic syndrome criteria (4)

A
  • peripheral oedema
  • proteinuria > 3g/ 24 hours
  • serum albumin < 25g/L
  • hypercholesterolaemia
164
Q

Most types of glomerulonephritis are treated with what 2 things?

A

Steroids - immunosuppression
ACE-i or ARBs - BP control, by blocking renin-angiotensin system

165
Q

What is the most common cause of nephrotic syndrome in children?

A

= minimal change disease

166
Q

Most common cause of nephrotic syndrome in adults?

A

= focal segmental glomerulosclerosis

167
Q

Histology: IgG + complement deposits on basement membrane. Is suggestive of which type of glomerulonephritis?

A

= membranous glomerulonephritis

168
Q

What is Goodpasture’s syndrome?

A

= rare condition where body produced anti-GBM (glomerular basement membrane) antibodies. Which attack the kidneys + lungs

169
Q

What antibody is present in Goodpasture’s syndrome?

A

= anti-GBM (glomerular basement membrane) antibodies

170
Q

Patient with acute interstitial nephritis presents with which 2 features?

A

= AKI + hypertension

171
Q

‘Muddy brown casts’ on urinalysis are suggestive of what condition?

A

= acute tubular necrosis

172
Q

Is acute tubular necrosis reversible?

A

= yes

173
Q

What is type 1 renal tubular acidosis?

(pathology is where, and what is unable to occur)

A

= pathology in distal tubule, unable to excrete hydrogen ions

174
Q

What is type 2 renal tubular acidosis?

(pathology is where, and what is unable to occur)

A

Pathology in proximal tubule, unable to reabsorb bicarbonate

175
Q

Type 4 renal tubular acidosis is caused?

A

= reduced aldosterone, can be caused by adrenal insufficiency, ACE-i, Spironolactone, SLE, diabetes, or HIV

176
Q

What is Fludrocortisone?

A

= mineralocorticoid, given in Addison’s and type 4 renal tubular acidosis to replace aldosterone is insufficient

177
Q

What is haemolytic uraemia syndrome (HUS)?

A

= occurs when there is thrombosis in small vessels throughout the body (formation of blood clots)

178
Q

Which bacteria toxin usually triggers haemolytic uraemia syndrome?

A

= shiga toxin

179
Q

Classic triad of patient presenting with haemolytic uraemia syndrome (HUS)

A
  • haemolytic anaemia
  • AKI
  • thrombocytopenia
180
Q

What is rhabdomyolysis?

A

= where skeletal muscle tissue breaks down and releases breakdown products into the blood

181
Q

What is diabetes insipidus due to?

A

Lack of anti-diuretic hormone (ADH) production, or lack of response to ADH

182
Q

What is vasopressin also known as?

A

= anti-diuretic hormone, ADH

183
Q

What are the 2 types of diabetes insipidus?

A
  • nephrogenic DI
  • cranial DI
184
Q

What is nephrogenic diabetes insipidus?

A

= when the collecting ducts of the kidney don’t respond to ADH

185
Q

What is cranial diabetes insipidus?

A

= when the hypothalamus doesn’t produce ADH for the pituitary gland to secrete

186
Q

How is diabetic insipidus diagnosed?

A

= water-deprivation test

187
Q

What is primary polydipsia?

A

= person drinks excessive amount of water, and therefore produces a lot of urine (ADH system is fully functioning)

188
Q

In cranial diabetes insidious, what would you expect the urine osmolarity to be: after water deprivation, and after desmopressin?

A

After water deprivation: low
After desmopressin: high

189
Q

In primary polydipsia, what would you expect the urine osmolarity to be: after water deprivation?

A

After water deprivation: high

190
Q

In nephrogenic diabetes insidious, what would you expect the urine osmolarity to be: after water deprivation, and after desmopressin?

A

After water deprivation: low
After desmopressin: low

191
Q

Management of cranial diabetes insipidus?

A

Demopressin (synthetic ADH) can be used to replace absent ADH

192
Q

Management of nephrogenic diabetes insipidus

A

Thiazide diuretics (to decrease urine volume)
Ensure plenty of water

Year 3 (10 decks)

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