Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Renal > Clin Med with some Phys and Biochem > Flashcards

Clin Med with some Phys and Biochem Flashcards

1
Q

Compare and contrast hypo- and hyperkalemia.

A

HypoK+ (<3.5):
S/S: Often asymptomatic, but can cause muscle weakness/cramping. In severe cases, flaccid paralysis, hyporeflexia, cardiac arrythmias.
Cause: Renal or GI loss
EKG: Flattening of T wave; less concerning than hyperK+

HyperK+ (>5.5):
S/S: Non-specific, but can cause fatal arrhythmias. Medical emergency
Cause: Often ESRD; possible low aldo (ACE/ARB) overdose
EKG: Peaked T waves, wide QRS

Stabilize with CaCl
Move K+ into cells with insulin & D50
Decrease total body K+ with kayexalate and loop diuretic

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

What are some common causes of hypernatremia?

A

Loss of free water (sweating, vomiting, or watery diarrhea); dehydration (esp. those dependent on others); or inadequate ADH (as in DI)

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

What are some common causes of hyponatremia?

A

Isotonic hyponatremia: lab artifact, lipids/proteins

Hypertonic hyponatremia: DM

Hypovolemic hypotonic hypoNa+: diuretics, GI loss, third spacing

Euvolemic hypotonic hypoNa+: SIADH; Addison’s

Hypervolemic hypotonic hypoNa+: cirrhosis, ascites, CHF, nephrotic syndrome (can’t excrete water)

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

Compare and contrast hyper- and hypocalcemia.

A

HypoCa2+: buzzword = Chvostek/Trousseau’s. Hyper-reflexia, tetany, possible convulsions

HyperCa2+: bradycardia, cramps, possible cardiac arrest

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

What’s the MC secondary cause of nephrotic syndrome?

A

DM

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

What are the MC causes of AKI?

A

Pre-renal or

Intra-renal:
In hospitalized patient, ATN
- secondary to contrast (MC)
- or ischemia after low perfusion event

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

Blood clots in urine

A

Extraglomerular hematuria

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

Dysmorphic RBCs in urine

A

Glomerular hematuria

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

Recent exposure to IV contrast, now presenting with signs of kidney injury

A

ATN (intrinsic AKI)

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

Muddy brown casts in UA

A

ATN (intrinsic AKI)

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

Kidney injury after cardiac catheterization

A

Vascular AKI

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

WBCs/white casts in UA

A

Interstitial AKI

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

Management of post-obstructive diuresis

A

Replace 3/4 of volume with 1/2 NS

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

Peaked T wave

A

HyperK+

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

Wide QRS complex

A

HyperK+

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

Flat T wave

A

HypoK+

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

Bradycardia and muscle cramps

A

HyperCa2+

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

Tetany and hyperreflexia

A

HypoCa2+

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

String of beads

A

Fibromuscular dysplasia, renovascular cause of secondary HTN

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

Refractory HTN in pt >50 YO

A

Athrosclerotic renal artery stenosis causing renovascular secondary HTN

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

Difference in pathophysiology of unilateral obstruction vs bilateral obstruction

A

Unilateral: initial AA dilation, then constriction
Bilateral: persistent EA constriction

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

Name the important transporters in the PT

A 
Na+/H+ Exchanger
Na+/HCO3- co-transporter
Na+/K+ ATPase
SGLT2/1 & GLUT2/1
Npt2a & Npt2c
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What effect does vitamin D have on Pi reabsorption?

A

Increases activity of Npt2a/c, increasing Pi reabsorption

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

What effect do FGF23 and PTH have on Pi reabsorption?

A

Decrease activity of the Npt2a/c, decreasing Pi absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Name the important transporters of the TAL of the LOH
``` Na+/H+ Exchanger NKCC K+ leak channel Na+/K+ ATPase CaSR (not a transporter, but important) ```
26
Name the important transporters of the DCT
NCC Na+/K+ ATPase Na+/Ca2+ exchanger TrpV5 Ca2+ channel
27
What effect do thiazide diuretics have on Ca2+ and why?
Thiazides inhibit NCCs in the DCT This causes less Na+ entry into the cell This allows the Na+/K+ pump/Na+/Ca2+ calcium cycle to operate more effectively This allows increased reabsorption of Ca2+
28
What effect does Vit D have on Ca2+ reabsorption in the DCT?
Vitamin D stimulates calbindin to "store" more Ca2+ in the cells of the DCT, allowing better reabsorption and less excretion back into the lumen
29
What effect does PTH have on the DCT?
PTH stimulates TrpV5 channels to allow more Ca2+ to be reabsorbed
30
Name the important transporters of the Principal Cells of the CD
ENaC ROMK/BK Na+/K+ ATPases
31
Name the important transporters of the Type-A Intercalated cells of the CD
H+ (secretory) H+/K+ exchangers Na+/K+ ATPases HCO3-/Cl- exchangers
32
How do Type B Intercalated cells differ from Type A?
They are essentially opposite, with Type B cells being active and upregulated in states of metabolic alkalosis
33
What are four triggers that cause muscle cells to move K+ into the cell?
Alkalosis (pushes H+ out of cell) Insulin B-agonists Aldosterone
34
What are four triggers that cause muscle cells to move K+ out of the cell?
Acidosis (bring H+ into the cell) Increased osmolarity (water rushes out of cell, brings K+) Intense exercise Cell lysis
35
Describe the location, mechanism, and manifestations of Fanconi syndrome.
Generalized deficiency of the transporters in the PT. Causes significant losses of electrolytes (hypokalemia). Causes metabolic acidosis because Na+/HCO3- co-transporter is not allowing effective reabsorption of bicarb.
36
Describe the location, mechanism, and manifestations of Bartter syndrome.
Deficiency of NKCCs in the TAL of LOH. Causes hypotension, RAAS activation (ineffective), hypokalemia, hypocalcemia, and alkalosis because Type A cells try to reclaim K+, but lose H+ in the process.
37
Describe the location, mechanism, and manifestations of Gitelman's syndrome.
Deficiency of NCCs in the DCT. Similar to Bartter syndrome but less severe: hypotension, RAAS activation, hypokalemia, hypocalcemia, and metabolic alkalosis (as Type A cells try to recapture K+ and lose H+ in the process)
38
Describe the location, mechanism, and manifestations of Liddle syndrome.
OVERACTIVITY of transporters in the CD. Causes hypertension without RAAS activation (little to no serum aldosterone); hypokalemia (overactive ROMK), and alkalosis.
39
When given an ABG, in what order are the values given, and what are the normal limits?
pH / CO2 / O2 / HCO3- ``` pH= 7.4 CO2 = 40 O2 = 90 HCO3- = 24 ```
40
When calculating acid/base status, what is normal pH?
7.4, +/- 0.05
41
When calculating acid/base status, what is normal PCO2?
40, +/-5
42
When calculating acid/base status, what is normal HCO3-?
24, +/- 2
43
When calculating acid/base status, what is the normal anion gap?
12, +/- 2
44
When anion gap is above ___, there is an AG-metabolic acidosis present
>14
45
What is indicated by a high excess anion gap?
Excess anion gap > 30 = metabolic alkalosis is present Excess anion gap <23 = non-anion gap metabolic alkalosis is present
46
What are causes of respiratory acidosis?
Anything that causes hypoventilation: opioid overdose, airway obstruction, COPD ...
47
What are causes of respiratory alkalosis?
Anything that causes hyperventilation Sepsis High altitude Salicylates
48
What are causes of anion-gap metabolic acidosis?
First guess: DKA, uremia, or methanol MUDPILES: methanol, uremia, DKA, paraldehyde, isoniazid, lactic acidosis, ethylene glycol, salicylates
49
What are causes of non-anion metabolic gap acidosis?
Diarrhea (GI loss of bicarb) Renal failure Increased serum Cl-
50
What are causes of metabolic alkalosis?
Vomiting/loss of gastric juices/NG tube suction K+ wasting diuretics Excess aldosterone Overuse of antacids
51
What is the location, degree of acidosis, potassium status, and pathophys of RTA type 1?
Location: Distal tubules Acidosis: Severe K+: Hypokalemia Pathophys: A-intercalated cells don't secrete H+
52
What is the location, degree of acidosis, state of K+, and pathophys of RTA type 2?
Location: PT Acidosis: Moderate K+: Hypokalemia Pathophys: failure to reabsorb bicarb in PT
53
What is the location, degree of acidosis, state of K+, and pathophys of RTA type 4?
Location: Adrenal glands Acidosis: Mild when present K+: Hyperkalemia Pathophys: low aldosterone or cells are resistant to aldosterone
54
Your patient has been in the hospital treated for excessive vomiting, and now has rising [Cr]. UA shows high specific gravity, high osmolarity, FENA <1%. What is the suspected diagnosis?
Pre-renal (volume loss) AKI.
55
What AKI presents with fever?
Interstitial renal AKI (inflammatory process)
56
Buzzword: Oval, Maltese cross-shaped fat bodies/fatty casts in UA
Nephrotic syndrome
57
What is the constellation of symptoms associated with nephrotic syndrome?
Proteinurea (> 3.5gm/day) Low albumin Hyperlipidemia Edema
58
Your patient presents with edema and her initial UA was remarkable for foamy urine and fatty casts. What is a good next step?
Suspicion of nephrotic syndrome: need to assess proteinurea. Start with a 24 hour collection, then spot UPCR/UACR to monitor. If any of these spots are suspect, confirm with another 24-hour collection.
59
One of the MC etiologies of CKD is DM: what is important to remember in managing CKD patients with DM?
Do not use metformin!!
60
What constitutes nephrotic range proteinurea?
> 3.5 gm/day
61
What constitutes sub-nephrotic range proteinurea?
150mg - 3.4gm/day
62
What are four things that can contribute to a false positive proteinurea test?
IV contrast (24 hours) Alkaline urine Gross hematuria Antiseptics used to clean perineum
63
What are three possible causes of benign proteinurea?
Isolated (no etiology, high CVD risk) Orthostatic (common in adolescents) Transient (exercise, UTI, fever -- repeat to confirm it passes)
64
What are the four categories of proteinurea?
Glomerular Tubular Overflow Post-renal
65
What are three triggers for ADH release?
AngII Increased plasma osmolarity Decreased pressure sensed by baroreceptors
66
What triggers renin release?
Decreased [NaCl] past macula densa
67
What are two triggers for aldosterone release?
AngII | High [K+]
68
What are two important uses for 1/2 NS?
Use as a maintenance fluid | Use in post-obstructive diuresis
69
Compare NS to RL
NS has more Na+, and no K+, HCO3-, or dextrose. It carries a higher risk of volume overload. It is used for emergent volume expansion. RL is more physiological than NS. DO NOT use in hyperK+ or hyperCa2+, as it contains these electrolytes.
70
What is the best fluid to give to a hypovolemic patient who has had upper GI fluid loss?
NS - more acidic than RL
71
What is the best fluid to give a hypovolemic patient who has had lower GI fluid loss?
RL - more alkaline than NS
72
What is the best fluid to give to a patient presenting with hypoglycemia, crackles, and edema?
D10 - used in volume overload + hypoglycemia

Renal (3 decks)

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