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Step 2 CK renal > R5 > Flashcards

R5 Flashcards

1
Q

Cause of bleeding in CKD?

A

Platelet dysfunction due to uremia
Defect in platelet endothelium and platelet with platelet interaction
Guanidinosuccinic accid is the major toxin

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2
Q

Laboratory finding?

A

Increase BT
Normal coagulation study
Normal platelet count
treat with desmopressin, cryoprecipitate, and conjugated desmopressin.

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3
Q

A drug used in MDR pyelonephritis that can cause AKI?

A

Amikacin by causing ATN

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4
Q

Tiazide use in hypercalciuria?

A

decrease urine ca level by increasing absorption in DCT

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5
Q

Distal symethric polynurophaty trigers?

A 
DM
Long-standing HIV
Uremia
toxins(alcohol, heavy metal, and chemotherapy(platinium based one)
B-12 deficiency
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6
Q

pathophysiology?

A

Damage to distal pheripherial nerve

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7
Q

manifestation?

A

Symptoms began in feet and toes
Symptoms progress over time
Distal numbness, tingling, pins, and needle sensation
Decrease pain, Temperature, touch, and vibration sensation.
Decrease ankle/Babinski reflex
Intact motor strength(spare motor neurons)

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8
Q

Treatment?

A 
Treat underlying cause
Pain managment
Gabapentine
TCA
Duloxetine
Capucine- cream
Acetaminophen-hydrocodone if not respond to the above medication
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9
Q

investigation to do inpatient with p.pnurophaty?

A

RBS
RFT
CBC( megaloblastic anemia)
PICT

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10
Q

HIV and P.Nurophaty?

A

Due to virus infiltration to sensory neuron–immune cell come to attack the neuron
Long-standing HIV, Low CD4, high viral load, using neurotoxic antiviral(didanosine and stavudine)
antiretroviral decrease disease progression

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11
Q

Effect and mechanism of renal compensation for respiratory alkalosis?

A

Increase renal H+ absorption and HCO3 excretion
High urine PH
Low serum HCO3

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12
Q

Characteristics of polyuria secondary to primary polydipsia?

A

Due to psychosis or antipsychotic(dry mouth)
IT is ADH-independent.
High urine osmolarity
No change to desmopressin treatment

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13
Q

Central DI cause?

A 
It is due to ADH deficiency
Trauma
Idiopathic
Pituitary surgery
Ischemic encephalopathy
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14
Q

urinary finding?

A

Low urine osmolarity but respond to desmopressinbut serum osmolarity rises with hypernatremia in water deprivation

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15
Q

Nephrogenic DI?

A 
Is due to ADH resistance
LIthium
Demeclocycline
Hypercalcemia
congenital defect
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16
Q

Finding?

A

Low serum osmolarity does not respond to desmopressin but serum osmolarity rises with hypernatremia in water deprivation

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17
Q

Diet-induced hyperkalemia?

A

Not expected in healthy adult

Can occur in a patient with renal failure and PAI

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18
Q

NS due to chronic inflammation is a result of?

A

Serum amyloid A protein accumulation

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19
Q

Heamodyalisis for hypercalcemia used?

A

Patients with ARF and CHF in which aggressive fluid managment is difficult.

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20
Q

Why biphosphonate delayed in hypercalcemia managment?

A

Its action delayed for 2-4 days

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21
Q

Glucocorticoid for hypercalcimia?

A

Used in case of hypercalcemia secondary to Vit D toxicity and sarcoidosis and certain lymphoma
Inhibit activated macrophages.

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22
Q

most sensitive test for albuminuria?

A

urine albumin-creatinine ratio test

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23
Q

diagnosis of DN?

A

persistent protinuria for > 3 month

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24
Q

managment?

A

ACE/ARB

SGCT II inhibitors (glifozins)

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25
Q

DI manifestation?

A

Sever polyuria
Euvolumic mild Hypernatrimia(normal high In NDI)
Hypoosmolar urine
Hyperosmolar serum

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26
Q

Cause of NDI?

A

hypercalcemia
sever hypokalemia
tubulointerstitial disease
Medication

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27
Q

medication?

A 
Lithium
Demeclocycline
Foscarnet
Cidofovir
Amphoteracine
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28
Q

myotonic dystrophy genetics?

A

Autosomal dominant
CTG trinuclotide repeat
Reapet lengeth inverseley proportionate with age

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29
Q

clinical fetcher?

A

myotonia(defective muscle relaxation)
progressive muscle weaknes(face and hand)
muscle wasting(atrophy)
childhood form: cognitive and behavioral problems)
Infantile form: Hypotonia and artherogryposis

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30
Q

associated finding?

A 
Arrhythmia
Cataract
Excessive daytime sleepiness
Testicular atrophy/infertility
sleep disturbance(executive daytime sleepiness)
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31
Q

Diagnosis?

A

Genetic testing

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32
Q

Treatment?

A

symptomatic
poor prognosis
patient die from respiratory or cardiac arrest at age 50-60

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33
Q

Hyperthyroidism weakness?

A

More proximal(hip flexors and quadriceps)

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34
Q

Renal vein thrombosis most common in which type of glomerulonephropathy?

A

membranous glomerulonephritis

35
Q

Lateral medullary(Wallenberg) syndrome CM?

A

Vestibular nucli(verigo,diplopia,nystagmus and vomiting)
Spinal trigeminal nuclin (Ipsilateral loss facial pain and temprature)
Inferior cerebral peduncl(ataxia)
Nucleus ambiguous(diminished gag reflex, dysphagia, and dysphonia)
Spinothalamic tract(contralateral loss of pain and temperature)
ipsilateral horner syndrome(Hypothalamic sympathetic fiber)

36
Q

Injured artery?

A

left vertebral artery

37
Q

conccusion clinical menifestation?

A

Transient nurologic deficiet (dizzines, disorentiationa, amnesia)
No structural nurologic injury

38
Q

Managment?

A

Remove the same day from physical play
Neurologic evaluation
Reset for >24 hr
Return to regular activity if symptoms resolve
physical activity; light aerobic exercise, non-contact sport, contact sport.
Neurocognitive: limited screen time and neurocognition

39
Q

when we need CT?

A

Skul fracture
anticoagulation
focal neurological deficit
amnesia for more than 30 min prior to injury

40
Q

when to return contact sport?

A

Not before 1 week

41
Q

early start associated with?

A

chronic traumatic encephalopathy

second impact syndrome

42
Q

AKI and diuretic therapy?

A

A diuretic can cause AKI especially it used for Corpumonale(Decrease CO)–hypotension –AKI(prerenal azotemia)

43
Q

classification for the cause of metabolic alkalosis?

A 
Saline responsive(Urine chloride < 20)
Saline non responsive(urine chloride  >20
44
Q

The saline responsive cause?

A 
Vomiting
Gastric suction
Diuretics
laxative abuse
Decrease oral intake
45
Q

saline resistant?

A 
Primary hyperaldostronism
Cushing disease
Severe hypokalemia(<2mEq/L)
46
Q

managment?

A

Treat the underline cause

Give normal saline for the responsive one

47
Q

A typical normal range of serum chloride?

A

96 to 106 milliequivalents per liter (mEq/L)

48
Q

How saline resistance cause result in high urine chloride?

A

High mineralocorticoid activity–high Na/H2O retention–High ECF–Kidney increase HCO3 and chloride secretion.

49
Q

Normal saline administration?

A

Treat hypochloremia and MA(by increasing HCo3 secreation)

50
Q

Present D/C inpatient with just CNS aneurism and aneurysm with rapture?

A

Aneurysm-specific CN palsy

With rapture–Associated severe headache

51
Q

Posterior Communicating artery aneurysm?

A

Oculomotor (both motor and sympathetic)

52
Q

Internal carotid or Anterior Communicating artery aneurysm?

A

CNII puls

53
Q

CN IV?

A

A.Superior cerebral artery

54
Q

CN VI?

A

A.Inferior cerebral artery

55
Q

What Faucher indicates hypertensive nephrosclerosis?

A 
Sign of chronic HTN(S4 sound & prominent apical impulse)
Shrunken kidney on ultrasound
Elevated creatinine
Bland urinalysis(No WBC and RBC)
Sign of CKD(like anemia)
Mild proteinuria (<1g/day
56
Q

Pathogenesis?

A

Chronic HTN—medial hypertrophy and intimal fibrosis—-Endothelial injury—leakage of plasma protein–hyaline arteriosclerosis–decrease renal B/F—glomerular/tubular necrosis & renal atrophy—glomerulosclerosis

57
Q

cause normal anion gap metabolic acidosis?

A 
HARDASS
Hyperchloremia/hyperalimentation
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
Fistula(pancreatic,ilocutanous..)
Urethral (diversion(e.g ilial loop)
58
Q

When to consider tubular disorder in CKD?

A

Hyperkalemia and non-anion gap MA unproportionate to renal dysfunction

59
Q

Why CKD patients did not HAVE MA until advanced (GFR<20)?

A

The remaining nephron compensates by increasing NH4 secretion to release H+ ion?

60
Q

Renal tubular acidosis feucher?

A

Non anion gap metabolic acidosis
Hyperkalemia
Common in an older patient with uncontrolled DM

61
Q

Pathogenesis?

A

Depend on type

62
Q

RTA type 4?

A

also called hyperkalemic RTA
Due to Hypoaldosteronism or aldosterone resistance;
or defective  NH3 synthesis in PCT Ž –defective - NH4+
excretion
Caused by  decreased aldosterone production (eg,
diabetic hypo reninism (JGC injury), ACE inhibitors, ARB, NSAIDs, heparin, cyclosporine, adrenal insufficiency) or aldosterone resistance (eg, K+-sparing diuretics, nephropathy due to obstruction(collecting duct injury, TMP-SMX)
Low urine PH and high serum K

63
Q

Defect in T1 RTA?

A

Inability of α-intercalated cells to secrete H+ -no new HCO– is generated metabolic acidosis

64
Q

Causes ?

A

Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, autoimmune diseases (eg, SLE)

65
Q

Characterized by?

A

High urine Ph(>5.5) and low k

66
Q

RTA 2?

A

Also called proximal renal tubular acidosis

67
Q

Cause?

A 
Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract,
autoimmune diseases (eg, SLE)
68
Q

Pathogenesis?

A

Defect in PCT HCO3 reabsorption—excessive excretion of HCO3 in urine –metabolic acidosis
Urine can be acidified by α-intercalated cells in collecting duct, but not enough to overcome  HCO3–
excretion

69
Q

Characteristic?

A

< 5.5 when plasma HCO3– below reduced absorption threshold
> 5.5 when filtered HCO3 exceeds absorptive threshold
Low potassium

70
Q

Caus?

A

Fanconi syndrome
multiple myeloma
carbonic anhydrase inhibitors

71
Q

Interstitial cystitis other name and epidimology?

A

Also called bladder pain syndrome
More common in females age >40
Assicited with psychiatric disorder and chronic pain disorder(fibromyalgia,IBD and endometriosis)

72
Q

clinical presentation?

A

Bladder pain with filling and relieved by voiding
Increase urinary urgency and frequency
Dysparunia
Chronic pelvic pain

73
Q

diagnosis?

A

Bladder pain >6 week w/o clear identified cause

Normal urinalysis

74
Q

Treatment?

A 
Not curetive
foccus on improving quality of life
bladder training
behavioural modification
avoid pricipitating factor like alcohol and caffiene
advance triger
physical therapy
amyitryptilin
pentosan polysulphate sodium
analgesic for acute exacerbation
75
Q

how to d/t from bladder diverticulum?

A

BD:Pain exacerbate with voiding and patient will have anterior vaginal mass

76
Q

renal infarction feucher?

A

Flank pain
hematuria
protinuria
no cast
wege shaped infarction on CT
elevated creatnin if large or bilateral infarction
elevated serum WBC .LDH and C-reactive protiene

77
Q

risk factor?

A

atrial fibrilation
hypercoagulable state
infective endocarditis

78
Q

Cause of redish in tuberclosis patient?

A

if normal urinalysis–rifamcpcine

if have RBC/WBC or protein in urinalysis-renal tuberculosis or TB realated gloumerlophaty

79
Q

Urinalysis in prerenal aothemia?

A

unremarkable( bland sediment)
fractional Na excretion <1 %
secreation <20

80
Q

Exersise induced hyponatremia CM?

A

Depend on hyponatremia severity
If mild:lethargy and nausea
sever:siezure and confusion

81
Q

pathophysiology?

A

occur in intense exersise like mharaton
mainley due to exesive water intake during or after exersise
thise patients also have temporary defect in dilute urine formation
The other mechanism is increase ADH during exersise due to ex.itself,pain ,hypoglycemia and nausea

prevent by apropriate wated usage during exersise

82
Q

An individual with a normal diet and normal fluid intake has a urine osmolality of ?

A

approximately 500-850 mOsm/kg water

83
Q

Cause of nephrotic syndrome?

A 
Minimal change disease(in children)
Membranous nephrophaty(in adult)
membranioproliferative disease
mesengial proliferative gloumerulonephritis
FSGN
84
Q

Complication of NS?

A

Hypercoagulablity(RVT the common)
Protien malnutrition
Iron resistance IDA(due to transferin loss)
Vit D deficiency:Due to loss of cholicalceferol binding protien
Decrease serum tyroxin due to Loss of TBG
Infection due to loss of immunoglobulins

Step 2 CK renal (5 decks)

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