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Step 2 CK renal > R5 > Flashcards

R5 Flashcards

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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
DI manifestation?
Sever polyuria Euvolumic mild Hypernatrimia(normal high In NDI) Hypoosmolar urine Hyperosmolar serum
26
Cause of NDI?
hypercalcemia sever hypokalemia tubulointerstitial disease Medication
27
medication?
``` Lithium Demeclocycline Foscarnet Cidofovir Amphoteracine ```
28
myotonic dystrophy genetics?
Autosomal dominant CTG trinuclotide repeat Reapet lengeth inverseley proportionate with age
29
clinical fetcher?
myotonia(defective muscle relaxation) progressive muscle weaknes(face and hand) muscle wasting(atrophy) childhood form: cognitive and behavioral problems) Infantile form: Hypotonia and artherogryposis
30
associated finding?
``` Arrhythmia Cataract Excessive daytime sleepiness Testicular atrophy/infertility sleep disturbance(executive daytime sleepiness) ```
31
Diagnosis?
Genetic testing
32
Treatment?
symptomatic poor prognosis patient die from respiratory or cardiac arrest at age 50-60
33
Hyperthyroidism weakness?
More proximal(hip flexors and quadriceps)
34
Renal vein thrombosis most common in which type of glomerulonephropathy?
membranous glomerulonephritis
35
Lateral medullary(Wallenberg) syndrome CM?
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
Injured artery?
left vertebral artery
37
conccusion clinical menifestation?
Transient nurologic deficiet (dizzines, disorentiationa, amnesia) No structural nurologic injury
38
Managment?
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
when we need CT?
Skul fracture anticoagulation focal neurological deficit amnesia for more than 30 min prior to injury
40
when to return contact sport?
Not before 1 week
41
early start associated with?
chronic traumatic encephalopathy | second impact syndrome
42
AKI and diuretic therapy?
A diuretic can cause AKI especially it used for Corpumonale(Decrease CO)--hypotension --AKI(prerenal azotemia)
43
classification for the cause of metabolic alkalosis?
``` Saline responsive(Urine chloride < 20) Saline non responsive(urine chloride >20 ```
44
The saline responsive cause?
``` Vomiting Gastric suction Diuretics laxative abuse Decrease oral intake ```
45
saline resistant?
``` Primary hyperaldostronism Cushing disease Severe hypokalemia(<2mEq/L) ```
46
managment?
Treat the underline cause | Give normal saline for the responsive one
47
A typical normal range of serum chloride?
96 to 106 milliequivalents per liter (mEq/L)
48
How saline resistance cause result in high urine chloride?
High mineralocorticoid activity--high Na/H2O retention--High ECF--Kidney increase HCO3 and chloride secretion.
49
Normal saline administration?
Treat hypochloremia and MA(by increasing HCo3 secreation)
50
Present D/C inpatient with just CNS aneurism and aneurysm with rapture?
Aneurysm-specific CN palsy | With rapture--Associated severe headache
51
Posterior Communicating artery aneurysm?
Oculomotor (both motor and sympathetic)
52
Internal carotid or Anterior Communicating artery aneurysm?
CNII puls
53
CN IV?
A.Superior cerebral artery
54
CN VI?
A.Inferior cerebral artery
55
What Faucher indicates hypertensive nephrosclerosis?
``` 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
Pathogenesis?
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
cause normal anion gap metabolic acidosis?
``` HARDASS Hyperchloremia/hyperalimentation Addison disease Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion Fistula(pancreatic,ilocutanous..) Urethral (diversion(e.g ilial loop) ```
58
When to consider tubular disorder in CKD?
Hyperkalemia and non-anion gap MA unproportionate to renal dysfunction
59
Why CKD patients did not HAVE MA until advanced (GFR<20)?
The remaining nephron compensates by increasing NH4 secretion to release H+ ion?
60
Renal tubular acidosis feucher?
Non anion gap metabolic acidosis Hyperkalemia Common in an older patient with uncontrolled DM
61
Pathogenesis?
Depend on type
62
RTA type 4?
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
Defect in T1 RTA?
Inability of α-intercalated cells to secrete H+ -no new HCO– is generated metabolic acidosis
64
Causes ?
Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, autoimmune diseases (eg, SLE)
65
Characterized by?
High urine Ph(>5.5) and low k
66
RTA 2?
Also called proximal renal tubular acidosis
67
Cause?
``` Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, autoimmune diseases (eg, SLE) ```
68
Pathogenesis?
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
Characteristic?
< 5.5 when plasma HCO3– below reduced absorption threshold > 5.5 when filtered HCO3 exceeds absorptive threshold Low potassium
70
Caus?
Fanconi syndrome multiple myeloma carbonic anhydrase inhibitors
71
Interstitial cystitis other name and epidimology?
Also called bladder pain syndrome More common in females age >40 Assicited with psychiatric disorder and chronic pain disorder(fibromyalgia,IBD and endometriosis)
72
clinical presentation?
Bladder pain with filling and relieved by voiding Increase urinary urgency and frequency Dysparunia Chronic pelvic pain
73
diagnosis?
Bladder pain >6 week w/o clear identified cause | Normal urinalysis
74
Treatment?
``` 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
how to d/t from bladder diverticulum?
BD:Pain exacerbate with voiding and patient will have anterior vaginal mass
76
renal infarction feucher?
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
risk factor?
atrial fibrilation hypercoagulable state infective endocarditis
78
Cause of redish in tuberclosis patient?
if normal urinalysis--rifamcpcine | if have RBC/WBC or protein in urinalysis-renal tuberculosis or TB realated gloumerlophaty
79
Urinalysis in prerenal aothemia?
unremarkable( bland sediment) fractional Na excretion <1 % secreation <20
80
Exersise induced hyponatremia CM?
Depend on hyponatremia severity If mild:lethargy and nausea sever:siezure and confusion
81
pathophysiology?
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
An individual with a normal diet and normal fluid intake has a urine osmolality of ?
approximately 500-850 mOsm/kg water
83
Cause of nephrotic syndrome?
``` Minimal change disease(in children) Membranous nephrophaty(in adult) membranioproliferative disease mesengial proliferative gloumerulonephritis FSGN ```
84
Complication of NS?
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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