Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Medicine > Renal And GUS > Flashcards

Renal And GUS Flashcards

(50 cards)

Start Studying
1
Q

criteria for nephrotic syndrome

A 
proteinuria >3.5g in 24h
hypoalbuminemia <3g/DL
generalised oedema
hyperlipidemia and lipiduria 
(hypercoagubility)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

criteria of nephritic syndrome

A

haematuria
hypertension
proteinuria (less than nephrotic)
oliguria and azotemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

size of largest molecules to be filtered in health

A

4nm (max diameter of gaps in podocytes) also +> - charge due to negative collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

mechanism of linear v granular immune deposits in glomeruli

A

linear: anti-GBM (TIV collagen alpha3 chain)
granular: circulating Ag (endogenous or exogenous) deposited OR Ab v GBM (to PLA2-R in membranous nephropathy only)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

exogenous antigens that can deposit in glomeruli

A

hep C At, HBsAg l, strep protein, treponema, plasmodium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

where are subendothelial deposits in the glomeruli

A

side near blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

where are subepithelial deposits in glomeruli

A

on the side near bowman’s capsule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Risk factors for Renal cell carcinoma?

A

Smoking, HTN, obesity
Acquired polycystic kidney disease (dialysis) RRx30
Occupational: cadmium, asbestos, pertrol
Chronic analgesia use (paracetamol, aspirin)
Family history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Age and sex for Renal cell carcinoma?

A

M>F. 60-80y

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Classical triad of RCC?

A

Haematuria
Abdominal pain
Flank mass
(Only present in 10%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Typical blood findings for RCC?

A

Anaemia (normocytic) + Raised ALP

Or Hypercalcaemia or polycythaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ways of RCC presentation?

A

Incidental finding
Classical triad: haematuria, abdo pain, flank mass
Local invasion: IVCO, Buddchiari, scrotal varicocoele, limb oedema
Paraneoplastic: anaemia, B symptoms, cahexia, lytic bone lesions, polycythaemia (EPO), feminisation, masculinisation, HTN, PMR, amyloidosis
Metastatic: (30% at present) lung, lymph, liver, bone, brain,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How would you investigate ?RCC

A 
Urine dip: haematuria (not great)
FBC: paraneoplastic syndrome
LDH: marker of advanced disease
LFTs + coag: metastases, Stauffer's syndrome
Corr Ca: raised (advanced disease)
U+Es
Imaging: US abdo/pelvis OR CT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is stauffer’s syndrome?

A

Non-metastatic (paraneoplastic) nephrogenic hepatic dysfunction. Cholestasis (elevated bilirubin, alk phos, GGT) + elevated PT, thrombocytosis and hepatosplenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

DDX for renal mass:

A

Benign: simple renal cysts (NB. USS to confirm not complex/malignant); or
Angiomyolipoma; or Oncocytoma.
Malignant: renal cell carcinoma, metastases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How to distinguish oncocytoma from RCC?

A

With difficulty! But management is similar anyway!
Mx: nephrectomy (to prevent complications/spont haemorrhage)
Biopsy: central stellate scar. Granular cytoplasm (looks like clear cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Subtypes of RCC?

A

Clear cell (65%)
Papillary renal cell (10-15%)
Chromophobe renal carcinomas (5%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Biochemistry of excess aldosterone?

A

Hypokalaemic, alkalosis, high to normal sodium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How to differentiate primary and secondary hyperaldosteronism?

A

Primary: normal-high Na, HTN, pH high. [renin] plasma LOW
Secondary: low Na (<138), ±HTN, pH maybe normal. (Look for causes: CCF, ascites, nephrotic syndrome) [renin] plasma HIGH
BOTH: K excretion >30mmol pd.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is Conn’s syndrome?

A

Primary adrenal disease with excess aldosterone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

signs and symptoms of Conn’s syndrome?

Study These Flashcards
A

Hypertension, muscle weakness, latent tenant, paraesthesia, polydipsia, polyuria, nocturia

22
Q

Cause of HTN + low K

Study These Flashcards
A

Thiazide diuretics

?conn’s syndrome

23
Q

How to investigate ?raised aldosterone?

Study These Flashcards
A

[aldosterone]/[renin]
Renin activity + renin mass
If both are low (<800, <80) excludes diagnosis
If both are high (>2000, >200) likely diagnosis

24
Q

How to confirm diagnosis of Conn’s syndrome?

Study These Flashcards
A
  1. Saline suppression test: 2l IVI 0.9% over 4h. Should decrease aldosterone. Diagnostic if aldosterone >140pmol/. (But risk of inducing cardiac failure esp in elderly)
  2. Sodium loading + fludrocortisone over 4d
    But needs admission to hospital and risks of serious hypokalaemia
25
Causes of conn's syndrome?
Adrenal adenoma Bilateral adrenal hyperplasia GC remediable hyperaldosteronism (genetic)
26
How to calculate plasma osmolality?
2x[Na] + [urea] + [glucose] (mmol/l)
27
Diagnostic criteria of SIAD
Hyponatraemia (<135) Hypo-osmolar plasma <270 Inappropriate concentrated urine >100mmol/kg No adrenal, renal ro thyroid dysfunction (Do NOT measure ADH, it's raised in most people with hyponatraemia anyway)
28
Causes of hyponatraemia?
(Sick cell, pseudo) Na losses (hypovolaemic) Inability to excrete free water (hypervolaemic) SIAD (normovolaemic)
29
Management of dilutional hyponatraemia?
(Correct at rate of onset, monitor carefully) Water restrict Demclocycline (v ADH-R antag @ collecting duct)
30
Risk of rapid correction of hyponatraemia?
Central pontine myelinolysis
31
Urgent correction of dilutional hyponatraemia?
Hypertonic saline (1.8/2.7/3%) to increase [Na] by 1mmol/l/h (Correct 0.5mmol/l/h if >48h onset) NOT if fluid overloaded.
32
Max increase of [Na]plasma per day?
Do NOT correct more than 10mmol/l over 24h.
33
When to stop treating urgent hyponatraemia?
When Na 120mmol/l or pt asymptomatic
34
How to correct dilutional hyponatraemia in fluid overloaded pt?
Loop diuretic + hypertonic saline?
35
Min Na, K, Cl intake pd?
1mmol/kg per day
36
Min water intake pd?
25-30ml/kg/day
37
Min glucose needed pd?
50-100g per day
38
Max K replacement?
<240mmol in 24h
39
What is Addison's disease?
Primary adrenal insufficiency. reduced aldosterone and cortisol.
40
How to distinguish hypervolaemic hyponatraemia due to CKD or CCF?
Urine osmolality: if >20mmol/l suggests renal cause. | Urine osmolality <20mmol/l suggests non-renal cause
41
Disorders associated with hypokalaemic alkalosis
Liddle's syndrome Gitelman's syndrome Bartter's syndrome
42
Baby presents with polyuria and low BP. Urinary Ca high. Na 138; K 2.8; Urea 3.4; Cr 62; pH 7.51; HCO3 33. Likely diagnosis?
Hypokalaemic Metabolic alkalosis. | Bartter's syndrome: salt wasting (hypercalciuria, Mg). Impaired Na resorption in LoH (NKCC2 defect)
43
What is Bartter's syndrome?
Defect in thick asc LoH. Direct/indirect impairment of NKCC2. Hypokalaemia, alkalosis, hypotension. Onset 24-30w. High renin and Aldosterone. Salt wasting: lose Ca, Mg, Cl, K in urine. PC: polyhydramnios, polyuria, polydipsia Autosomal recessive
44
What is Liddle's syndrome?
Activating mutation in ENaC (DCT Na channel): always active. Pseudohyperaldosteronism. Retain Na and H2O PC: infant-early adult. Autosomal dominant. HTN, hypernatraemia, hypokalaemia (high HCO3, low renin and aldosterone)
45
4 ways NSAIDs kill the kidneys
Dysregulation of blood flow Toxic Tubulointerstitial insult Membranous GN Minimal change GN
46
Cause of patchy tubular necrosis?
Renal hypoperfusion/prerenal AKI.
47
Causes of confluous tubular necrosis?
Exogenous: solvents, gentamycin, heavy metals, radiocontrast Endogenous: HbC, myoglobin, light chain (myeloma)
48
Stages of AKI?
1: 1.5xincrease in [Cr] (>0.3mg/dl) OR <0.5ml/kg/h for 6h 2. 2-3xincrease in [Cr] OR <0.5ml/kg/h for >12h 3. >3xincrease in [Cr] OR <0.5ml/kg/h for >24h OR anuria for 12h OR renal replacement therapy needed
49
Indications for dialysis?
``` AEIOU Acidosis Electrolytes (K) Ingested toxins Overload Uraemic ```
50
Stages of CKD?
(GFR in ml/min) 1: >90 + something else e.g. ACR>3 2. 60-90 3. 30-59 4. 15-49 5. <15 AKA ESRF

Medicine (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions