Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 > Renal > Flashcards

Renal Flashcards

1
Q

How many nephrons in each kidney?

A

800,000 to 1,200,000

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

What forms the filtration slits in the renal corpuscle?

A

Podocytes - pedicles project.

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

What are the two capillary beds of the nephron?

A

Glomerular, peritubular

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

What % of cardiac output do the kidneys receive?

A

20%

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

What is the normal filtration rate of the kidneys?

A

180L/day

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

How much water is excreted in urine under normal conditions?

A

1.5L

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

Functions of the kidney? (6)

A

Volume/BP, concentration, pH, metabolic, excretory, endocrine

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

Simply, how do the kidneys control blood volume?

A

Excretion or retention of fluid

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

What ions do kidneys maintain the concentration of? (7)

A

Sodium (Na+), potassium (K+), chloride (Cl-), magnesium (Mg2+), hydrogen (H+), bicarbonate (HCO3+), calcium (Ca2+)

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

Which ions are regulated in the kidney to control blood pH?

A

H+, acidic. HCO3+, alkalotic.

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

What role do the kidneys play in metabolism? (2)

A

A small amount of gluconeogenesis, activate vitamin D from 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D

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

What endocrine function do the kidneys serve? (2)

A

Production of erythropoietin, renin production (RAAS system)

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

What excretory function do the kidneys serve? (3)

A

Excreting - metabolic waste inc. urea & creatinine, water-soluble drugs, toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What 3 types of balance do the kidneys maintain?

A

Acid-base, fluid, electrolyte

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

What does the GFR stand for and what does it mean?

A

Glomerular filtration pressure - net filtration pressure across glomerular capillaries.

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

What blood vessels control blood flow & hydrostatic pressure in the intervening glomerular capillary?

A

Afferent & efferent arterioles.

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

Increased resistance in the afferent arteriole has what effect?

A

Lower renal blood flow, lower net ultrafiltration pressure

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

Increased resistance in the efferent arteriole has what effect?

A

Lower renal blood flow, higher net ultrafiltration pressure

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

Sympathetic stimulation/norepinephrine release has what effect on the renal arterioles?

A

Vasoconstriction of afferent AND efferent arterioles - resistance in both rises, generally decreasing RBF & GFR.

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

Generally, what effect does angiotensin II have on the renal arterioles?

A

Vasoconstriction of afferent AND efferent arterioles.

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

What do prostaglandins help prevent occurring in the kidneys?

A

Severe & potentially harmful vasoconstriction, renal ischaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What effect do prostaglandins have on the renal arterioles?

A

Dampens the vasoconstrictive effects of sympathetic nerves of angiotensin II, especially on the AFFerent arterioles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What stimulates the release of natriuretic peptides?

A

ANP & BNP released in response to increased pressure & circulating volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the myogenic response, and which arteriole does it affect?

A

Constriction in response to pressure - prevents vessel from being stretched, increases vascular resistance, and therefore prevents excessive increases in renal blood flow & GFR with BP rises. Affects the AFFerent arteriole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is tubule-glomerular feedback, and what effect does it have?

A

Increased arterial pressure increases GFR, which results in more Na+ & Cl- in the proximal tubule - this is sensed by the macula densa cells. These release paracrine agents to the AFFerent arteriole, triggering contraction and increasing vascular resistance - counteracts initial GFR increase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the range of pH in body tissues?

A

7.35 to 7.45

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What two processes generate acid & alkali in the body?

A

Diet & metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is an acid?

A

H+ donor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is a base?

A

H+ acceptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is a weak acid?

A

HA <-> H+ & A- = partial dissociation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is a weak base?

A

B & H+ <-> BH+ = partial dissociation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What time frame of adjustment to pH changes do kidneys need vs lungs?

A

Kidneys - days (metabolic) - lungs - rapid (respiratory)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the definition of a buffered solution?

A

Addition of an acid or base does not affect the pH of the solution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How do weak acids buffer?

A

The conjugate base (A-) of the partially dissociated weak acid (HA) neutralises the added acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How do weak bases buffer?

A

The hydrogen ion (H+) from the partially dissociated weak base (BH+) neutralises added alkali

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Name some physiological buffers (4)

A

Bicarbonate (HCO3-), phosphate (H2PO4-) & (HPO4^2-), plasma proteins, haemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the bicarbonate buffer system?

A

CO2 + H2O <-> H2CO3 <-> H+ + HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Which step of the bicarbonate buffer system is the slow step?

A

CO2 + H2O <-> H2CO3. Catalysed by carbonic anhydrase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Which step of the bicarbonate buffer system is the quick step?

A

H2CO3 <-> H+ + HCO3-. Fast ionisation reaction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What effect does increased CO2 in the blood have on pH?

A

pH decreases - acidosis!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Definition of acidemia?

A

An arterial pH below the normal range

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Definition of alkalemia?

A

An arterial pH above the normal range

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Definition of acidosis?

A

A process that tends to lower the pH of extracellular fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Definition of alkalosis?

A

A process that tends to raise the pH of extracellular fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is NEAP?

A

Net Endogenous Acid Production (50-100mmol/day) - necessitates reclamation of filtered bicarbonate, and generation of new bicarbonate to neutralise the daily acid load.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is secreted for every bicarbonate ion reabsorbed or generated in the tubules?

A

A H+ ion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What would happen to urinary HCO3- excretion if a carbonic anhydrase-inhibiting drugs is administered?

A

Missing catalyst slows the slow step of the bicarbonate buffer. The bicarbonate is not reabsorbed. More HCO3- excreted in the urine. results in metabolic acidosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What does focal refer to in glomeruli?

A

Only some glomeruli affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What does segmental refer to in glomeruli?

A

Part of the glomerulus is affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What does diffuse refer to in glomeruli?

A

All glomeruli affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What does global refer to in glomeruli?

A

The whole glomerulus is affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What does cell proliferation mean?

A

Increase in the number of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What does cell expansion mean?

A

Increase in intercellular matrix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What does crescent refer to in glomeruli?

A

Proliferation of cells within Bowman’s space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the cause of intrinsic glomerulonephritis?

A

Antibody to the intrinsic glomerular antigens. e.g. Goodpastures, T4 collagen antibodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the cause of painted glomerulonephritis?

A

Antibody binds to ‘planted’ glomerular antigens. e.g. post-strep glomerulonephritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the cause of circulating complex glomerulonephritis?

A

Deposition of circulating antigen-antibody complexes. e.g. lupus nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is non-specific glomerulonephritis?

A

Non-specific deposition of circulating antibody. e.g. IgA nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Indications for renal biopsy? (5)

A

Nephrotic syndrome (adults), renal dysfunction of unknown cause (esp. acute), to guide treatment/assess prognosis when diagnosis is known, dysfunctional transplant kidney, sometime haematuria or proteinuria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Contraindications to renal biopsy? (6)

A

Abnormal clotting/thrombocytopenia, drugs (aspirin, clopidogrel, warfarin, DOACs), uncontrolled hypertension (e.g. >170/100), single kidney, hydronephrosis, UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What 3 analyses are performed on renal biopsies?

A

Light microscopy (basic morphology/cellular infiltrate, special stains e.g. silver for collagen), Immunostaining (immunoglobulin or complement components), electron microscopy (ultrastructural detail,, including immune deposits)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Definition of nephrotic syndrome? (3)

A

Proteinuria (>3.5g/day), hypoalbuminaemia, oedema (& hyperlipidaemia, hypercoagilability)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Definition of nephritic syndrome? (5)

A

Haematuria, mild/moderate proteinuria, hypertension, oliguria, red cell casts in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

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

A

Minimal change disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Treatment for minimal change disease?

A

Steroids (may relapse, may require heavier immunosuppression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Causes of minimal change disease? (3)

A

Idiopathic, drugs (e.g. NSAIDs), lymphoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Presentation of Focal Segmental Glomerulosclerosis (FSGS)?

A

Nephrotic syndrome +/- renal impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Treatment for FSGS?

A

Steroids, immunosuppression - much less responsive than minimal change disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Causes of FSGS? (5)

A

Primary. Secondary - obesity, IV heroin use, HIV, drugs (e.g. pamindronate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Biopsy appearance of FSGS? (3)

A

Focal involvement, segmental sclerotic lesion, C3 & IgM deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

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

A

Membranous nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Biopsy appearance of membranous nephropathy? (2)

A

‘Spikes’ on basement membranes, IgG deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Associated with membranous nephropathy? (3)

A

Malignancy, drugs (e.g. gold, penicillamine, captopril), infections (e.g. hepatitis, malaria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is the prognosis for membranous nephropathy? (3)

A

Rule of 3rds. 1/3 improve spontaneously, 1/3 stay the same, 1/3 develop progressive disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Treatment for membranous nephropathy?

A

Immunosuppression - may respond.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Presentation of mesangiocapillary glomerulonephritis?

A

Nephritic or nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Biopsy of MCGN? (3)

A

Mesangial proliferation, thickened capillary walls (double contouring of basement membranes), positive immunofluorescence (e.g. C3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Associated with MCGN? (3)

A

Infections (e.g. hepatitis, malaria, endocarditis, shunt nephritis), cryoglobulinaemia, malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Can MCGN recur after kidney transplantation?

A

Yes

79
Q

What commonly shows on histology in diabetic nephropathy?

A

Kimmelstiel-Wilson lesions - modular glomerulosclerosis

80
Q

Clinical features of diabetic nephropathy? (3)

A

Initial low level proteinuria (microalbuminuria), heavier proteinuria (may be nephrotic), progressive decline in GFR

81
Q

What is AL amyloidosis?

A

Light chain deposition, e.g. myeloma

82
Q

What is AA amyloidosis?

A

Chronic inflammation, e.g. infection, CTD

83
Q

What stain is used in amyloidosis?

A

Congo red - apple green birefringence under polarised light, with visible fibrils on microscopy.

84
Q

How can renal amyloidosis present? (3)

A

Heavy proteinuria +/- nephrotic syndrome, +/- renal failure

85
Q

What is Berger’s disease?

A

IgA nephropathy

86
Q

What is the most common form of glomerulonephritis?

A

IgA nephropathy

87
Q

Presentations of IgA nephropathy? (3)

A

Asymptomatic microscopic haematuria, episodic macroscopic haematuria (e.g. exercise, respiratory tract infection), progressive renal impairment/end stage renal failure. Presentations sooner that post-strep GN (after 2-3 days)

88
Q

Associations with IgA nephropathy? (2)

A

Liver disease, Henoch-Schönlein purpura

89
Q

Pathophysiology of IgA nephropathy?

A

Deposition of circulating IgA within the mesangium - leads to expansion of mesangial matrix, mesangial cell proliferation.

90
Q

Presentation of post-strep GN?

A

2-3 weeks after a Group A strep infection (e.g. throat, skin), usually nephritic.

91
Q

Biopsy findings post-strep GN? (4)

A

Neutrophil infiltration, mesangial & epithelial cell proliferation, IgG & C3 deposition, sub epithelial deposits

92
Q

Treatment for post-strep GN?

A

Supportive care

93
Q

Name two systemic vasculitides that can cause pouch-immune glomerulonephritis?

A

Wegener’s granulomatosis/granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA)

94
Q

Biopsy findings renal vasculitis? (2)

A

Focal necrotising glomerulonephritis, crescents on biopsy

95
Q

Treatment for vasculitic glomerulonephritis? (2)

A

Immunosuppression +/- plasma exchange

96
Q

What antibodies cause Goodpasture’s/anti-GBM?

A

Antibodies to type 4 collagen

97
Q

Presentation of Goodpasture’s? (2)

A

AKI, pulmonary haemorrhage. Rapid course.

98
Q

Biopsy findings Goodpasture’s? (2)

A

Focal necrotising glomerulonephritis, crescents on biopsy but linear antibody deposition

99
Q

Treatment for Goodpasture’s? (2)

A

Immunosuppression, plasma exchange

100
Q

Presentation of rapidly progressive glomerulonephritis/crescentic nephritis? (2)

A

Nephritic syndrome, rapidly deteriorating renal function

101
Q

Biopsy findings RPGN? (2)

A

Acute inflammatory process with crescent formation, cellular proliferation in Bowman’s space.

102
Q

How many classifications of lupus nephritis are there, and what are they?

A

6 - normal glomeruli inc. minimal change, mesangial disease, focal proliferation, diffuse proliferation, membranous nephropathy, advanced sclerosis

103
Q

Urine investigations? (4)

A

Dipstick (blood, protein, nitrites, leukocytes, nitrites, pH), microscopy (cells, casts, crystals), culture, protein quantification (24h collection)

104
Q

Bloods for renal investigation? (4)

A

Haematology (FBC, ESR, coag, blood film), biochemistry (U&Es, LFTs, Ca, PO4, CRP), immunology (autoantibodies e.g. ANA, ANCA, anti-GBM, etc. Serum immunoglobulins & electrophoresis, Serum free light chains, Cryoglobulins, Complement levels), microbiology (blood cultures, serology e.g. hepatitis B/C, HIV, ASO titre/strep)

105
Q

Imaging for renal investigation? (6)

A

CXR, renal USS, CT, MRI, angiography, nuclear medicine

106
Q

Proteins in urine? (3)

A

Albumin, LMW proteins (beta-2 microglobulin, polypeptides, RBP), secreted proteins

107
Q

What are the abnormal thresholds for ACR & PCR respectively?

A

ACR >3, PCR >15

108
Q

What are the nephrotic range ACR & PCR values?

A

ACR >250, PCR >300

109
Q

Types of benign proteinuria? (2)

A

Orthostatic proteinuria (children & adolescents, <3.5g/day), transient proteinuria - secondary to fever, heavy exercise, vasopressor, IV albumin (<1g/day)

110
Q

Primary glomerulonephritides? (5)

A

Minimal change disease, Primary FSGS, Idiopathic membranous nephropathy, IgA nephropathy, Idiopathic membranoproliferative glomerulonephritis/MPGN

111
Q

Secondary glomerulonephritides (6)

A

Diabetes mellitus, systemic amyloidosis, Secondary FSGS (e.g. obesity, HPTN, HIV), Autoimmune disease (e.g. SLE), Secondary membranous nephropathy (e.g. cancer, drugs), MPGN (hepatitis B/C)

112
Q

Where in the nephron are LMW proteins processed? (2)

A

Filtered at the glomerulus, reabsorbed in the proximal tubule

113
Q

What is overflow proteinuria?

A

Excess production of LMW proteins, exceeds reabsorptive capacity of tubules

114
Q

What can cause overflow proteinuria? (3)

A

Myeloma (free light chains), rhabdomyolysis (myoglobin), haemolysis (haemoglobin)

115
Q

What can cause post-renal proteinuria? (2)

A

Inflammation or lower urinary tract - infection, stones.

116
Q

What two things is proteinuria a known risk factor for?

A

Cardiovascular disease, progressive CKD

117
Q

Why does nephrotic syndrome include thrombosis risk?

A

Decreased concentrations of antithrombin III & plasminogen

118
Q

General management for nephrotic syndrome? (5)

A

Low sodium diet & fluid restriction, diuretics, RAAS inhibition & blood pressure control, statin, anticoagulation

119
Q

Nephrotoxic drugs? (13)

A

ACEI, ARB, diuretics, methotrexate, statin, gentamicin, vancomycin, bisphosphonates, calcineurin inhibitors (e.g. ciclosporin, tacrolimus), lithium, mesalazine, NSAIDs, CT contrast

120
Q

At what week does the ‘permanent’ kidney form, and what is it called?

A

Week 5, metanephros

121
Q

What is renal genesis?

A

One or both kidneys fail to develop

122
Q

What is pelvic kidney?

A

A kidney fails to ascend, is stuck in pelvis. Can function normally. Ureter could cause strangulation.

123
Q

What is horseshoe kidney?

A

The kidneys are fused together at the lower end or bases.

124
Q

What is the function of ACE/angiotensin converting enzyme?

A

Converts angiotensin I to angiotensin II

125
Q

Where does renin act?

A

Conversion of angiotensinogen to angiotensin I.

126
Q

What increases release of renin? (4)

A

Low arterial BP, low BP in glomerular blood vessels, increased loss of Na+/water, increased sympathetic activity

127
Q

What decreases release of renin? (3)

A

Na+/water retention, increased BP, activation of AT1 (angiotensin II type I) receptors (short loop negative feedback

128
Q

What 3 things control renin secretion?

A

Macula densa pathway, intrarenal baroreceptor pathway, beta-receptor pathway

129
Q

Where is renin stored & secreted from?

A

Juxtaglomerular cells in granules.

130
Q

How does the intrarenal baroreceptor pathway affect renin release?

A

Detected increase in BP or renal perfusion pressure in preglomerular vessels - inhibits renin release.

131
Q

What type of feedback loop are renin and angiotensin II in?

A

Short loop negative feedback. Increased renin causes increased angiotensin II.

132
Q

What pharmacological agents decrease renin release? (3)

A

NSAIDs (inhibit PG synthesis), centrally acting sympatholytic agents & beta blockers (reduce beta-receptor activation), ACEI/ARB/renin inhibitors

133
Q

How do loop diuretics affect renin release?

A

Decrease BP, and increase NaCl reabsorption - causes increased renin release.

134
Q

What enzymes act as an alternative pathway for angiotensinogen -> AngI or directly AngII? (5)

A

Cathepsin, tonin, cathepsin G, chymostatin-sensitive angII generating enzyme, heart chymase

135
Q

What does angiotensin II rapid pressor response do? (2)

A

Constricts AFFerent arterioles, weak vasoconstriction in splanchnic vessels, brain, lungs, and skeletal muscle.

136
Q

What does angiotensin II slow pressor response do? (5)

A

Reduces urinary excretion of Na+/water, increases excretion of K+, stimulates Na+/H+ exchange in the proximal tubule (increases Na+, Cl- & bicarb reabsorption), increases Na+ glucose symporter in proximal tubule expression, directly stimulates Na+/K+/2Cl- symporter in the thick ascending limb

137
Q

Effects of aldosterone antagonists? (3)

A

Na+/water loss, hyperkalaemia, acidosis risk

138
Q

What is classed as mild hyponatremia?

A

130-135mmol/L

139
Q

What is classed as moderate hyponatremia?

A

125-129mmol/L

140
Q

What is classed as profound hyponatremia?

A

<125mmol/L

141
Q

Presentation of acute hyponatremia? (3)

A

Seizures, coma, respiratory distress - severe cerebral oedema

142
Q

Presentation of chronic hyponatremia? (7)

A

Frequently mild/asymptomatic, headache, restlessness, muscle cramps, nausea & vomiting, lethargy, confusion & disorientation - adaptation minimises cerebral oedema, risk of injury from over-treated hyponatremia!

143
Q

What condition does overly rapid hyponatremia correction put the patient at risk of?

A

Central pontine myelinosis/osmotic demyelination syndrome

144
Q

What is TURP syndrome?

A

Trans-urethral resection of prostate - too much hypotonic irrigation fluid is absorbed into the bloodstream during the operation, results in volume overload.

145
Q

Management of TURP syndrome? (4)

A

Supportive care of cardiac & respiratory functions (including airway protection if necessary), fluid restriction, furosemide, hypertonic saline.

146
Q

What is SIADH?

A

Syndrome of Inappropriate Antidiuretic Hormone Secretion - results in hyponatremia with hypervolaemia or euvolaemia

147
Q

What is ADH also known as?

A

Vasopressin

148
Q

What causes SIADH? (9)

A

Central nervous system disorders (trauma, psychosis, stroke, infection, haemorrhage), malignancy (especially small cell lung cancer), drugs (e.g. carbamazepine, SSRIs, cyclophosphamide), surgery (pain afferents?), pulmonary disease (pneumonia, atelectasis, asthma, pneumothorax), hypopituitarism/hypothyroidism, vasopressin/desmopressin/oxytocin, HIV, hereditary

149
Q

What drugs commonly cause hyponatremia? (8)

A

Thiazides, amiloride, carbamazepine, sulphonylureas (NOT gliclazide), PPIs, SSRIs & antidepressants, ACEI & ARBs, opiates

150
Q

What is beer potomania?

A

Patient with low daily solute intake & excessive beer consumption (which is low in sodium) - euvolaemic hypotonic hyponatremia

151
Q

Diagnostic criteria for SIADH? (6)

A

Effective serum osmolality <275mOsm/kg, urine osmolality >100mOsm/kg, clinical euvolaemia, urine Na+ >30mmol/L with normal dietary salt & water intake, absence of adrenal/thyroid/pituitary/renal insufficiency, no recent diuretic use.

152
Q

Hyponatremia assessment? (8)

A

Water gain & water loss, confirm not pseudohyponatremia, identify any heart/liver/kidney failure, check if on thiazide diuretics, assess volume status, compare urine & serum osmolality, urinary sodium, TFTs/AM cortisol/ACTH stimulation

153
Q

What is pseudohyponatremia?

A

Spuriously low serum Na+ with normal serum osmolality. Check for additional solute that may affect lab result.

154
Q

What are the 5 Rs of adult IV fluid therapy?

A

Resuscitation, Redistribution, Routine maintenance, Replacement, Reassessment

155
Q

What are some examples of redistribution in consideration for IV fluids? (4)

A

Oedema, hypoalbuminaemia/low oncotic pressure, sepsis, acute pancreatitis (third-spacing)

156
Q

Clinical signs of shock? (8)

A

Low systolic blood pressure (<100mmhg), BPM >90, RR <20, delayed capillary refill time (>2s), cool peripheries, high/deteriorating EWS (early warning score), response to passive leg raise/PLR, confusion/decreased/loss of consciousness

157
Q

What is a bolus of IV fluids in a normal pt? ml & mins?

A

500ml - 15 mins

158
Q

At what ml given should you seek expert assistance when you have been delivering IV fluids?

A

2000 - 2L or more.

159
Q

What is a colloid fluid?

A

A fluid with lots of starch/protein components

160
Q

How many ml/kg body weight/day do normal people need of water?

A

25-30ml/kgbw/day

161
Q

How many mmol/kgbw/day of sodium, potassium, and chloride do normal people need?

A

1-2mmol/kgbw/day

162
Q

How many g of glucose per day does a normal person need?

A

50-100g/day

163
Q

Normal 0.9% saline - how many mmol or g Na+, K+, Cl-, HCO3-, Glu?

A

Na+ 154, K+ 0, Cl- 154, HCO3- 0, Glu 0g

164
Q

5% dextrose - how many mmol or g Na+, K+, Cl-, HCO3-, Glu?

A

Na+ 0, K+ 0, Cl- 0, HCO3- 0, Glu 50g

165
Q

Hartmann’s solution - how many mmol or g Na+, K+, Cl-, HCO3-, Ca2+, Glu?

A

Na+ 131, K+ 5, Cl- 111, HCO3- 29, Ca2+ 2 Glu 0g

166
Q

What should be taken into account when calculating fluids? (3)

A

How much is being lost - urination, vomiting, diarrhoea, stoma output, NG tube output. How much is going in - oral intake of liquid & food, medications, IV administration, surgery. Inappropriate fluid loss - third-spacing, bleeding, oedema, etc.

167
Q

What can excessive vomiting cause?

A

Hypochloraemic/hypokalaemic metabolic alkalosis.

168
Q

How do you correct hpochloraemic/hypokalaemic metabolic alkalosis?

A

Supplemental K+ & Cl-

169
Q

What two ions are predominantly lost in ileum via stoma or fistula?

A

Na+, Cl-

170
Q

Where is the primary distribution for 5% glucose solution IV?

A

Intracellular

171
Q

Where is the primary distribution for colloids IV?

A

Plasma volume

172
Q

Where is the primary distribution for 0.9% normal saline?

A

Interstitial & lymphatics, also plasma volume.

173
Q

pH of normal saline 0.9%?

A

4.5-7

174
Q

pH of 5% glucose/dextrose?

A

3.5-5.5

175
Q

pH Hartmann’s?

A

5-7

176
Q

When would you consider using Human Albumin Solution (HAS) 4.5%/20% for fluid resuscitation? (4)

A

Severe sepsis, therapeutic plasma exchange, large-volume paracentesis (3L), hepato-renal syndrome

177
Q

Treatment for hypovolaemic hyponatremia?

A

Continuous normal saline, regular U&Es monitoring

178
Q

Treatment for euvolaemic hyponatremia?

A

Consider SIADH - fluid restriction, usually <1L/day. Paired urine & serum osmolality.

179
Q

Treatment for hypervolaemic hyponatremia? (3)

A

HoWater restriction, consider diuretics if overload symptomatic - <6mmol/day correction, SLOW.

180
Q

How to manage fluid resus in CKD/dialysis patients? (2)

A

SMALL boluses with reassessment of fluid responsiveness every time. Potassium/phosphate restricted (even calcium, sodium) - consider this.

181
Q

What form of calcium is not excreted by the kidneys?

A

Protein-bound

182
Q

Total serum calcium

A

Ionised (active) calcium + protein-bound calcium

183
Q

What does adjusted calcium give a better idea of?

A

Ionised calcium levels

184
Q

What should also be considered alongside calcium level?

A

Serum albumin

185
Q

What is released when low serum calcium is detected by parathyroid gland receptors?

A

PTH is released

186
Q

What effect does PTH have? (5)

A

Acts on distal convoluted tubule = more calcium reabsorption, increases osteoclastic activity, more intestinal calcium absorption, increased bit D hydroxylation/activation, more phosphate excretion

187
Q

Vitamin D relevance to calcium levels?

A

Activates osteoblasts, which stimulate osteoclasts - calcium release

188
Q

What effect does calcitonin have?

A

Opposite of PTH - reduces PTH, decreases vitamin D activation on detection of hypercalcaemia.

189
Q

What supplement do you give to CKD patients with vitamin D deficiency?

A

Calcitriol

190
Q

Why do you give calcitriol in CKD for vit D deficiency?

A

Activated vitamin D - bypasses the activation step in the kidneys.

191
Q

Causes of hypocalcaemia? (3)

A

Hypoventilation, alkalosis (bind more ionised Ca2+!), decreased intake (GI, bones, excess loss, inadequate intake)

192
Q

Causes of hypercalcaemia? (3)

A

Excess intake, excess loss from bones, increased mobilisation from bones

193
Q

Calcium has what effect on muscle contraction?

A

More calcium delays depolarisation (slowing action potential, less muscle contraction), less increases depolarisation (more muscle contraction)

194
Q
A

Year 3 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions