R5 Flashcards
Cause of bleeding in CKD?
Platelet dysfunction due to uremia
Defect in platelet endothelium and platelet with platelet interaction
Guanidinosuccinic accid is the major toxin
Laboratory finding?
Increase BT
Normal coagulation study
Normal platelet count
treat with desmopressin, cryoprecipitate, and conjugated desmopressin.
A drug used in MDR pyelonephritis that can cause AKI?
Amikacin by causing ATN
Tiazide use in hypercalciuria?
decrease urine ca level by increasing absorption in DCT
Distal symethric polynurophaty trigers?
DM Long-standing HIV Uremia toxins(alcohol, heavy metal, and chemotherapy(platinium based one) B-12 deficiency
pathophysiology?
Damage to distal pheripherial nerve
manifestation?
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)
Treatment?
Treat underlying cause Pain managment Gabapentine TCA Duloxetine Capucine- cream Acetaminophen-hydrocodone if not respond to the above medication
investigation to do inpatient with p.pnurophaty?
RBS
RFT
CBC( megaloblastic anemia)
PICT
HIV and P.Nurophaty?
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
Effect and mechanism of renal compensation for respiratory alkalosis?
Increase renal H+ absorption and HCO3 excretion
High urine PH
Low serum HCO3
Characteristics of polyuria secondary to primary polydipsia?
Due to psychosis or antipsychotic(dry mouth)
IT is ADH-independent.
High urine osmolarity
No change to desmopressin treatment
Central DI cause?
It is due to ADH deficiency Trauma Idiopathic Pituitary surgery Ischemic encephalopathy
urinary finding?
Low urine osmolarity but respond to desmopressinbut serum osmolarity rises with hypernatremia in water deprivation
Nephrogenic DI?
Is due to ADH resistance LIthium Demeclocycline Hypercalcemia congenital defect
Finding?
Low serum osmolarity does not respond to desmopressin but serum osmolarity rises with hypernatremia in water deprivation
Diet-induced hyperkalemia?
Not expected in healthy adult
Can occur in a patient with renal failure and PAI
NS due to chronic inflammation is a result of?
Serum amyloid A protein accumulation
Heamodyalisis for hypercalcemia used?
Patients with ARF and CHF in which aggressive fluid managment is difficult.
Why biphosphonate delayed in hypercalcemia managment?
Its action delayed for 2-4 days
Glucocorticoid for hypercalcimia?
Used in case of hypercalcemia secondary to Vit D toxicity and sarcoidosis and certain lymphoma
Inhibit activated macrophages.
most sensitive test for albuminuria?
urine albumin-creatinine ratio test
diagnosis of DN?
persistent protinuria for > 3 month
managment?
ACE/ARB
SGCT II inhibitors (glifozins)
DI manifestation?
Sever polyuria
Euvolumic mild Hypernatrimia(normal high In NDI)
Hypoosmolar urine
Hyperosmolar serum
Cause of NDI?
hypercalcemia
sever hypokalemia
tubulointerstitial disease
Medication
medication?
Lithium Demeclocycline Foscarnet Cidofovir Amphoteracine
myotonic dystrophy genetics?
Autosomal dominant
CTG trinuclotide repeat
Reapet lengeth inverseley proportionate with age
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
associated finding?
Arrhythmia Cataract Excessive daytime sleepiness Testicular atrophy/infertility sleep disturbance(executive daytime sleepiness)
Diagnosis?
Genetic testing
Treatment?
symptomatic
poor prognosis
patient die from respiratory or cardiac arrest at age 50-60
Hyperthyroidism weakness?
More proximal(hip flexors and quadriceps)
Renal vein thrombosis most common in which type of glomerulonephropathy?
membranous glomerulonephritis
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)
Injured artery?
left vertebral artery
conccusion clinical menifestation?
Transient nurologic deficiet (dizzines, disorentiationa, amnesia)
No structural nurologic injury
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
when we need CT?
Skul fracture
anticoagulation
focal neurological deficit
amnesia for more than 30 min prior to injury
when to return contact sport?
Not before 1 week
early start associated with?
chronic traumatic encephalopathy
second impact syndrome
AKI and diuretic therapy?
A diuretic can cause AKI especially it used for Corpumonale(Decrease CO)–hypotension –AKI(prerenal azotemia)
classification for the cause of metabolic alkalosis?
Saline responsive(Urine chloride < 20) Saline non responsive(urine chloride >20
The saline responsive cause?
Vomiting Gastric suction Diuretics laxative abuse Decrease oral intake
saline resistant?
Primary hyperaldostronism Cushing disease Severe hypokalemia(<2mEq/L)
managment?
Treat the underline cause
Give normal saline for the responsive one
A typical normal range of serum chloride?
96 to 106 milliequivalents per liter (mEq/L)
How saline resistance cause result in high urine chloride?
High mineralocorticoid activity–high Na/H2O retention–High ECF–Kidney increase HCO3 and chloride secretion.
Normal saline administration?
Treat hypochloremia and MA(by increasing HCo3 secreation)
Present D/C inpatient with just CNS aneurism and aneurysm with rapture?
Aneurysm-specific CN palsy
With rapture–Associated severe headache
Posterior Communicating artery aneurysm?
Oculomotor (both motor and sympathetic)
Internal carotid or Anterior Communicating artery aneurysm?
CNII puls
CN IV?
A.Superior cerebral artery
CN VI?
A.Inferior cerebral artery
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
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
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)
When to consider tubular disorder in CKD?
Hyperkalemia and non-anion gap MA unproportionate to renal dysfunction
Why CKD patients did not HAVE MA until advanced (GFR<20)?
The remaining nephron compensates by increasing NH4 secretion to release H+ ion?
Renal tubular acidosis feucher?
Non anion gap metabolic acidosis
Hyperkalemia
Common in an older patient with uncontrolled DM
Pathogenesis?
Depend on type
RTA type 4?
also called hyperkalemic RTA
Due to Hypoaldosteronism or aldosterone resistance;
or defective NH3 synthesis in PCT –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
Defect in T1 RTA?
Inability of α-intercalated cells to secrete H+ -no new HCO– is generated metabolic acidosis
Causes ?
Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, autoimmune diseases (eg, SLE)
Characterized by?
High urine Ph(>5.5) and low k
RTA 2?
Also called proximal renal tubular acidosis
Cause?
Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, autoimmune diseases (eg, SLE)
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
Characteristic?
< 5.5 when plasma HCO3– below reduced absorption threshold
> 5.5 when filtered HCO3 exceeds absorptive threshold
Low potassium
Caus?
Fanconi syndrome
multiple myeloma
carbonic anhydrase inhibitors
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)
clinical presentation?
Bladder pain with filling and relieved by voiding
Increase urinary urgency and frequency
Dysparunia
Chronic pelvic pain
diagnosis?
Bladder pain >6 week w/o clear identified cause
Normal urinalysis
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
how to d/t from bladder diverticulum?
BD:Pain exacerbate with voiding and patient will have anterior vaginal mass
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
risk factor?
atrial fibrilation
hypercoagulable state
infective endocarditis
Cause of redish in tuberclosis patient?
if normal urinalysis–rifamcpcine
if have RBC/WBC or protein in urinalysis-renal tuberculosis or TB realated gloumerlophaty
Urinalysis in prerenal aothemia?
unremarkable( bland sediment)
fractional Na excretion <1 %
secreation <20
Exersise induced hyponatremia CM?
Depend on hyponatremia severity
If mild:lethargy and nausea
sever:siezure and confusion
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
An individual with a normal diet and normal fluid intake has a urine osmolality of ?
approximately 500-850 mOsm/kg water
Cause of nephrotic syndrome?
Minimal change disease(in children) Membranous nephrophaty(in adult) membranioproliferative disease mesengial proliferative gloumerulonephritis FSGN
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
