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4th year blocks > Internal > Flashcards

Internal Flashcards

1
Q

Define prerenal AKI?

Give 8 examples

A

Any injury leading to decreased renal perfusion

Hypovolemia
Hypotension 
Cardiorenal syndrom 
Hepatorenal syndrom 
Abdominal compartment syndrom 
Acute pancreatitis 
Drugs 
Renal artery stenosis
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2
Q

Define intrinsic AKI?

Give 4 examples

A

Conditions leading to severe and direct renal damage

Acute tubular necrosis
Acute interstitial nephritis
Vascular diseases
GN: RPGN

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3
Q

Define Postrenal AKI

Give 8 examples

A 
Acquired obstruction 
BPH 
Iatrogenic (catheter injuries) 
Tumors 
Stones 
Bleeding causing blood cloth 
Neurogenic bladder 
Congenital malformations
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4
Q

Causes of ATN?

A

Ischemia
Nephrotoxic drugs
Endogenous toxins: Hb in hemolysis, Mb in rhabdomyolysis, uric acid in tumor lysis, Bence-Jones protein light chains in MM

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5
Q

Define Hemolytic uremic syndrom? (HUS)

A

thrombotic microangiopathy occluding the microvasculature

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6
Q

what is hepatorenal syndrom?

A

Liver cirrhosis - portal HT - increased speelic artery vasodilators (NO) - decreased BP - RAAS activation - renal vasoconstriction - decreased GFR

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7
Q

what is abdominal compartment syndrom?

A

increased pressure in the abdomen causing compression of vessels

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8
Q

vascular injuries in interstitial AKI (6)

A 
HUS
TTP 
HT crisis 
vasculitis 
scleroderma 
renal vein infarct
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9
Q

define AKI

A

acute/sudden decrease in renal function withing hours to 7 days (creatinine/urinary output)

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10
Q

Normal creatinine level?

A

60-99

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11
Q

diagnosis of AKI

A
  1. patient history
  2. Physical examination
  3. lab test - stage with creatinine
  4. pre, intrinsic or post
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12
Q

what can you calculate to differentiate Prerenal and intrinsic renal AKI?

A

FeNa: (Pre <1%) (Intrinsic >2-3%)
FeUrea: (Intrinsic > 50%)

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13
Q

Define CKD

A

Chronic kidney disease (CKD) is defined as an abnormality of kidney structure or function that persists for > 3 months

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14
Q

most common causes of CKD (5)

A
  1. Diabetic nephropathy
  2. Hypertensive nephropathy
  3. Glomerulonephritis
  4. PKD
  5. NSAIDs
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15
Q

inflammatory GN?

A
  1. RPGN
  2. PSGN
  3. SLE nephritis
  4. HUS
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16
Q

Non-inflammatory GN?

A

MCGN
Membranous nephropathy
FSGN

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17
Q

what happens in our body when CKD?

A
  1. decreased urin production - volume retention
  2. no toxin excretion - uremia
  3. hyperphosphatemia (when FGF23 subsides)
  4. amenia due to EPO insufficiency
  5. HPTH
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18
Q

What can uremia do in the heart?

A

uremic pericarditis - fibrinous pericarditis

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19
Q

Define end stage kidney disease?

is it reversible?

A

GFR < 15 mL/min

not reversible

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20
Q

What disease can we frequently see in CKD and have to treat?

A

Osteodystrophy due to hyperphosphatemia, hypocalcemia and vit D deficiency causing hyperparathyroidism

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21
Q

Indications of dialysis?

A 
Acidosis 
Electrolyte disorder - hyperkalemia 
Intoxication 
Overload of fluids 
Uremic syndrom (pericarditis)
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22
Q

Nephritic syndrom presentation

A 
proteinuria < 3.5 
hematuria - acanthocytes 
RBC casts in urin might be seen 
no edema/general little 
proliferative 
hypertension due to oliguria
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23
Q

nephrotic syndrom?

A 
proteinuria > 3.5 
no hematuria 
edema 
hyperlipidemia 
non-proliferative
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24
Q

why is there a increased risk of thromboembolism in nephrotic syndrom?

A

loss of antithrombin III

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25
Q

causes of nephrotic syndrom? (6)

A
  1. MCD
  2. FSGS
  3. membranous nephropathy
  4. diabetic nephropathy
  5. amyloid light chain AL amiloidosis
  6. lupus nephritis
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26
Q

Causes og nephritic syndrom (9)

A
  1. PSGN
  2. RPGN
  3. Lupus nephropathy
  4. IgA nephropathy
  5. granulomatosis with polyangiitis
  6. microscopic polyangiitis
  7. good pasture syndrom
  8. Alport syndrom
  9. Thin basement membrane
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27
Q

systemic symptoms of RPGN

A 
fever 
weight loss
joint pain 
weakness 
palpable purpuras
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28
Q

treatment of minimal change disease

A

good respons to steroids

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29
Q

treatment of FSGS

A

long steroid treatment

cyclosporins if steroid resistant

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30
Q

membranous nephropathy treatment

A

steroid + cyclophosphamides/cyclosporin

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31
Q

treatment of diabetic nephropathy

A

ACEI/ARBs to control BP and proteinuria

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32
Q

treatment of amyloidosis

A

hematogenic treatment

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33
Q

labs in PSGN

A

Anti-streptolysin titer
Low C3/Normal C4
Elevated IgM and IgG/normal IgA

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34
Q

lab parameters in ANCA vasculitis RPGN

A

elevated anti-MPO
elevated ant-PR3
eosinophilia
normal complement level

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35
Q

lab tests in Good-Pasture RPGN

A

anti-GBM
rarely ANCA positivity
normal complement

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36
Q

IgG deposits on immunofluorecent in Good-pasture RPGN?

A

LInear deposition

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37
Q

labs in SLE nephritis

A 
ANA-positivity 
elevated anti-dsDNA 
elevated anti-C1q 
low C3 and C4 
potential pancytopenia
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38
Q

immunofluorecent in SLE nephritis

A

FULL HOUSE

granular Ig G, A, M, C3, C1q

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39
Q

oliguria value?

A

< 400 ml urine /day

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40
Q

Diagnosis in acute tubulointerstitial diseases, treatment?

A

Biopsy

treatment depends on cause but corticosteroids in almost every case

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41
Q

caused of acute TIN

A

drugs
infection
systemic infection
idiopathic

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42
Q

name the tubulointerstitial diseases (4)

A
  1. Acute TIN
  2. MM cast nephropathy
  3. isolated tubulopathies
  4. renal tubular acidosis
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43
Q

what is the most common kidney injury in multiple myeloma (MM)

A

multiple myeloma cast nephropathy

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44
Q

pathophysiology of MM cast nephropathy?

A

light chains are filtered and excreted in urine
they precipitate in tubules clogging them
obstruction and toxic to tubular cells

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45
Q

forms of isolated tubulopathies

A

Fanconi and

Gitelman

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46
Q

pathophysiology in Gitelman syndrome?

A

like the patient is taking continous Thiazides

Na wast - no K+ exchange - hypokalemia - alkalosis

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47
Q

Fanconi syndrom pathophysiology

A

impaired bicarbonate reabsorption

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48
Q

what other diseases does ARPKD manifest with?

A

pulmonary insufficiency

progressive liver failure - portal and hepatic fibrosis

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49
Q

what other diseases does ADPKD manifest with?

A

arterial hypertension

progressive liver disease

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50
Q

curative treatment of PKD

A

transplantation

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51
Q

mutation in ADPKD

A

PKD1 ch 16 - polycystein-1

PKD2 ch 4 polycystein-2

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52
Q

mutation in ARPKD

A

PKHD1 ch 6 - fibrocystin

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53
Q

mechanism of PKD1 and PKD1

A

PKD1 - cell-cell / cell-matrix interaction
PKD2 nonselective cation channel transporter Ca2+
renal cysts in medulla and cortex compressing vessels activation RAAS

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54
Q

PKHD1 mutation mechanism

A

defect fibrocystin - cystic dilation of collecting duct and bile ducts (intrahepatic and extrahepatic)

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55
Q

where may the cysts also be in ADPKD

A

pancreas, liver, ovary and testicle

hepatic benign cysts increases with age

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56
Q

what is important to monitor in ADPKD if family history of stroke?

A

barrys aneurism - subarachnoid bleeding

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57
Q

what can be seen in children born with ARPKD?

A

potter syndrom during pregnancy (no embryo urin)
clubbed feet
craniofacial abnormalities

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58
Q

what is the difference between the cysts in AR and ADPKD on US?

A

both bilateral but AD varying in size and AR same size

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59
Q

whend do you use MRI in PKD?

A

to screen for berry’s aneurysms if family history

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60
Q

what mediation can slow down a rapid progression of ADPKD

A

tolvaptan

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61
Q

which medication should not be given in polycystic kidney disease?

A

ADH - increase cyst growth

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62
Q

risk factors for renal cell carcinoma (7)

A 
smoking 
acquired cysts 
nephrolithiasis 
long term acetaminophen use
hepatitis C 
HT 
Sickle cell anemia
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63
Q

when does RCC usually become symptomatic?

A

tumor size > 10 cm and/or if merastasis is present

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64
Q

causes of calcium oxalate stones

A

hypercalcemia
hyperoxaluria
hypocitraturia

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65
Q

causes of uremic acid stones

A

hyperuricemia - hyperuricosuria
increased cell turnover (leukemia, chemo)
gout

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66
Q

cause of calcium phosphate stones

A

hyper parathyroidism

type 1 tubular acidosis

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67
Q

clinical symptoms of urinary tract stones

A 
unilateral colicky pain 
radiates to the groin 
progressive worsening 
hematuria 
nausea, vomiting, reduced bowel sounds 
dysuria, frequency, urgency,
passing stones 
unable to sit still
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68
Q

if imaging is needed in nephrolithiasis which?

A

CT without contrast - hydronephrosis

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69
Q

what imaging is used in follow up after nephrolithiasis treatment?

A

KUB X-ray (kidney, ureter, bladder)

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70
Q

is x-ray always good in nephrolithiasis?

A

not for small stones

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71
Q

when do you consult with nephrology in UTI stones?

A

if size > 10mm

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72
Q

what analgesic is given in nephrolithiasis?

A

diclofenac

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73
Q

conservative treatment of nephrolithiasis?

A
  1. Tamsulosin (alpha blocker) if < 10 mm

2. Nifedipine (CCB)

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74
Q

Interventional treatment of nephrolithiasis?

A

ureteroscopy (URS) or
extracorporeal shockwave lithotripsy (ESWL)

renal stones larger then 20 mm percutaneous nephrolithotomy

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75
Q

indication of a glomerular hematuria?

A 
light color/normal color urine 
acanthocytes 
RBC cast might be seen 
no cloths 
proteinuria > 500mg/day
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76
Q

indication of non-glomerular bleeding

A 
dark urine 
no acanthocytes 
no RBC casts 
cloths might be seen 
proteinuria < 500mg/day mostly albumin
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77
Q

normal protein excretion?

A

up to 200mg/day

mostly Tomm Horsfall proteins from LOH

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78
Q

normal albumin excretion

A

< 30mg/day

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79
Q

proteinuria level

A

> 150mg/day urin

just remember that it IS normal up to 200mg/day

80
Q

normal protein in a spot urin test?

A

20 mg protein/ mmol creatinine
3g albumin/mmol creatinine

100mg/mmol spot urin corr to 1g/day proteinuria

81
Q

clinically significant proteinuria?

A

> 500mg/day

so on a spot test that is 50mg

82
Q

indication of renal biopsy?

A
  1. nephrotic syndrome
  2. nephritic syndrom
  3. RPGN
  4. asymptomatic proteinuria (1-3g/day)
  5. AVI if not ATN
  6. CKD (if US does not show small scarred kidneys)
  7. dysfunction after transplant
83
Q

contraindications of renal biopsy

A
  1. uncooperative patient
  2. one kidney
  3. multiple cysts
  4. renal neoplasia
  5. acute pyelonephritis
  6. uncontrolled bleeding
  7. uncontrolled BP (165/95)
84
Q

two types of esophageal diverticula and their cause?

A

pulsion diverticula: increased P and decreased relaxation og LES causing fals diverticula

Traction diverticula: mediastinal inflammation, scarring and retraction (tuberculosis or fungi)

85
Q

most common site of esophageal diverticula?

A

UES (Zenker)
middle 3rd
epiphrenic

86
Q

indications of esophageal diverticula

A 
dysphagia 
food regurgitation 
halitosis (bad breath) 
coughing when eating 
retrosternal pressure and pain 
weight loss 
neck mass
87
Q

types of hiatal hernia

A
  1. sliding
  2. paraoesophageal
  3. mixed
  4. multiorgan
88
Q

when is reflux defined as GERD?

A

when it causes troublesome symptoms and complications

89
Q

3 types of GERD

A

NERD (non-erosive)
ERD
Barret esophagus

90
Q

treatment of GERD?

A

start giving PPI and see if it gives a response, if yes then GERD if no do an EGDC to confirm and do a 24h esophageal pH monitoring

91
Q

what esophageal pH indicated GERD

A

dropp below 4

92
Q

surgical method in GERD

A

fundoplication where the fundus if stomach is wrapped around the lower esophagus narrowing the distal esophagus

93
Q

how many biopsies to take to diagnose Barret esophagus?

A

8 random - if negative repeat after 1-2 years

94
Q

endoscopic ablative techniques in Barret esophagus

A
  1. EMR - endoscopic mucosal resection
  2. ESD - endoscopic submucosal dissection
  3. RFA - radiofrequency ablation
95
Q

what is eosinophilic esophagitis?

how is it diagnosed?

A

Allergen induced inflammation of the esophagus

biopsy of upper and lower part showes > 15 eosinophils/HPF

96
Q

what is achalasia?

A

degeneration of the meienteric plexus of the lower 2/3 esophagus + failure to relax LES

97
Q

two types of achalasia

A

primary - unknowns etiology

secondary - mechanical cause

98
Q

causes of secondary achalasia

A
  1. esophageal tumor
  2. gastric tumor
  3. chagas disease
  4. amyloidosis
  5. sarcoidosis
  6. neurofibromatosis type 1
99
Q

what type of dysphagia is seen in achalasia?

A

dysphagia to solids AND fluids

100
Q

what is the difference between esophageal obstruction vs achalasia?

A

in obstruction dysphagia only to solids but achalasia to both

101
Q

diagnosis achalasia?

A

Barium swallowing test
endoscopy
manometry
CX-ray

102
Q

treatment of achalasia

A

surgery: hellers myotomy

surgical risk: botulnum toxin

103
Q

what is Boerhaave syndrom

A

spontaneous transmural effort rupture of esophagus (sudden increase in esophageal pressure)

104
Q

examples of etiology for boerhaave syndrom

A

forcefull vomiting (ex. after alcohol)
childbirth
prolonged coughing
seizures

105
Q

gold standard in boerhaave syndrom diagnosis?

A

esophagography with contrast showing contrast leaked

106
Q

define Mallory Weiss syndrom

A

upper GI bleeding due to longitudinal mucous tear at gastroesophageal junction (may continue above or below also)

107
Q

4 predisposing factors for Mallory Weiss syndrom?

A

alcohol
bulimia
GERD
hiatal hernia

108
Q

diagnosis of Mallory Weiss

A

CBC
pretransfusion testing - blood transfusion
ECG ro rule out ACS
EGD to confirm diagnosis

109
Q

type of gastritis and their main cause?

A

Acute: bacteria, fungi, virus, Parasite

Chronic: autoimmune type 1 and H. pylori type 2
causes destruction of the native architecture

Athropic: chronic inflammation with destruction of glands, fibrosis and scarring

Erosive: stress or chemicals causing multiple superficial erosions not extending beyond muscularis

110
Q

what are the toxic virulence of H. pylori

A

cytotoxic associated gene A (CagA)

Vacuolating cytotoxin A (VacA)

111
Q

treatment of H. pylori

A

2x1 PPI
clarithromycin 2x500mg
amoxicillin 2x1g or metronidazole 3x500mg

112
Q

define a peptic ulcer

A

defect in the gastric or duodenal mucosa with a diameter > 0.5 cm a depth reaching the muscularis mucosa

113
Q

what protects the gastric mucosa from the acidic environment?

A

HCO3- and mucus secretion

114
Q

what factors can increase to make a peptic ulcer?

A

increased pepsin or acid release or disruption of protective mechanism

115
Q

etiology of peptic ulcer disease

A 
gastric acid hypersecretion 
nervous system dysfunction 
genetic factors (inherited hyperpepsinogenemia) 
environmental factors (alcohol, smoking, eating habits, NSAID, stress)
116
Q

where does H. pylori most frequently cause an ulcer?

A

70-90% duodenum

30-60% stomach

117
Q

what cause of peptic ulcer is more likely to present with symptoms?

A

NSAID usage

118
Q

symptomatic differentiation between duodenal and gastric ulcers

A

gastric ulcers: increased pain after eating + weight loss

dudenal ulcer: decreased pain after eating + weight gain

119
Q

histamin effect on gastric acid?

A

increases secretion

120
Q

treatment of peptic ulcers?

A

antacids
H2R
PGL
PPI

121
Q

define gastroparesis

A

altered emptying > 3 months with no mechanical obstruction

122
Q

small for size syndrom

A

liver resection, jaundice, encephalopathy, coagulopathy

123
Q

most common medication giving acute liver failure

A

acetaminophen (paracetamol)

124
Q

what is the dominant symptom in hyperacute liver failure

A

encephalopathy is the main presentation and jaundice is mild, this can cause late diagnosis

125
Q

levels of hepatic encephalopathy

A

level 1 mild with no to very mild clinical presentations

level 5 coma

126
Q

define Preeclampsia

A

Preeclampsia is a pregnancy complication characterized by high blood pressure and signs of damage to another organ system, most often the liver and kidneys

127
Q

define Eclampsia

A

Eclampsia is a severe complication of preeclampsia. It’s a rare but serious condition were high blood pressure results in seizures during pregnancy.

128
Q

why is liver biopsy commonly contraindicated?

A

due to significant risk of bleeding

129
Q

hepatitis B treatment

A

entecavir and tenofovir

130
Q

what to give in a liver intoxication with acetaminophen?

A

N-acetylcystein

131
Q

acute steps in liver failure patients?

A
  1. fluids
  2. vasopressors if nonresponsive to fluids
  3. treat ARDS (seen in 20%)
  4. Do early intubation of rapidly progressing HE
  5. Start Spo2 monitoring and give oxygen in needed
  6. check for AKI (seen in 30-70%)
  7. dialysis if needed
132
Q

treatment of hepatic encephalopathy

A 
Lactulose (to remove ammonia from system) 
Rifampicin (in minimal HE) 
Metronidazole 
Vancomycin 
Electrolyte supplement if needed 
Nutrition
133
Q

pancreatitis 2/3 rule

A
  1. epigastric pain
  2. laboratory studies (x3 normal value)
  3. imaging (CT/US/MRI)
134
Q

What is used to decide severity of pancreatitis?

A

SIRS score and BISAP score

135
Q

what is used on a pancreatitis BISAP score?

A 
se urea 
mental state 
SIRS criteria 
age 
hydrothorax
136
Q

what are the SIRS criteria

A 
core temp 
HR 
RR 
PaCO2 
WBC
137
Q

what is decided with the pancreatitis BISAP score?

A

< 2 points means mortality is less then 2%

> 2 points means mortality is > 15%

138
Q

what can a sudden decrease in Hct during an acute pancreatitis indicate?

A

pancreatic hemorrhage (rare)

139
Q

what is a worsening of leukocytosis in pancreatitis an indication of?

A

infected necrosis

140
Q

what can be an indication of severe necrotizing pancreatitis?

A

CRP > 150 three days after onset
increased procalcitonin
increased IL-6
LDH high

141
Q

indications of chronic alcoholism

A

GGT high

MCV above 100fL

142
Q

what is a more specific biliary obstruction enzyme?

A

ALP

ALT > AST

143
Q

fluid replacement in acute pancreatitis?

A

rapid early replacement 5-10ml/kg/h
ringer lactate solution
monitor efficacy

144
Q

what lab parameter informs us about hydration and rehydration? (5)

A 
Hematocrit!! 35-45%
urea production 
BP 
HR 
MAP
145
Q

what parameters is misleading in the early state of pancreatitis?

A

CRP and WBC rise in the beginning due ti STERILE inflammation - this is not an indication for AB treatment

Procalcitonin PCT is the ONLY indicator of an actual infection if the patient has acute pancreatitis

146
Q

why is ERCP only recommended to use in case of AP with cholangitis?

A

it has the highest complication rate in endoscopy

147
Q

when to do a cholecystectomy in ABP with peripancreatic fluid?

A

safe after 6 weeks

148
Q

local complications of pancreatitis

A

AP fluid collection
pancreatic pseudocyst
acute necrotic collection
pleural effusion

149
Q

pathophysiology in chrons

A

dysfunction of IL-23 and Th17

150
Q

IBD extraintestinal skin manifestations

A

pyoderma gangrenosum

erythema nodosum

151
Q

Fistulas in chrons and UC?

A

Chrons: common
UC: rare

152
Q

complications in Chron?

A

abscess
strictures - obstruction
perianal fissures

153
Q

antibody in Chron?

A

ASCA

154
Q

abdominal pain location in Chrons vs UC

A

LLQ - UC

RLQ - Chrons

155
Q

complications in ulcerative colitis

A

Fulminant colitis
toxic megacolon
perforation

156
Q

antibody in ulcerative colitis

A

pANCA

157
Q

where in the GI do you NOT see chrons disease?

A

Rectum

158
Q

what are often the first sign of chrons?

A

perianal fistulas and abscesses

159
Q

what can be seen on a biopsy (histology) of Chron disease?

A

crypts and granulomas

160
Q

preferred imaging in Chrons

A

Cross sectional enterography

161
Q

what does steroid-resistant Chrons disease mean

A

when you give 40-60mg/day prednisone and there is no respons after 30 days

162
Q

what does steroid dependent chrons disease mean?

A

when there is a clinical respons within 30 days of 25mg/day prednisone

163
Q

90% of patients with primary sclerosing cholangitis are also infected with…..

A

Ulcerative colitis

but not the other way around

164
Q

what is elevated on a lab test of UC if there is also primary sclerosing cholangitis

A

GGT

165
Q

types of ulcerative colitis?

A 
proctitis 
proctosigmoiditis 
distal colitis 
extensive colitis 
pancolitis
166
Q

treatment of distal ulcerative colitis?

A

mesalamine

steroids

167
Q

treatment of extensive ulcerative colitis

A 
mesalamin 
sulfasalazine 
budesonide
steroids 
immunosupression
168
Q

Surgical treatment of ulcerative colitis?

can surgery in CD cure the disease?

A

Ileal pouch-anal anastomosis (IPAA)
curative intent

(CD cannot be cured with surgery)

169
Q

types of microscopic colitis?

A

lymphatic MC

Collagenous MC

170
Q

what should be stopped if a patient is diagnosed with microscopic colitis?

A

NSAID because it triggers it

171
Q

mutation in celiac disease?

A

HLA- DQ2 90%

HLA DQ8 10%

172
Q

serological tests in celiac disease

A

anti-Tg (IgA, IgG)
EMA (IgA, IgG
Deaminated glutamin peptide (DGP - IgG)

173
Q

how to diagnose celiac disease?

A

4 our of 5 rule

  1. signs and symptoms
  2. Ab testing
  3. HLA gene positive
  4. histology: villous atrophy and crypt hyperplasia
  5. clinical respons to gluten free diet
174
Q

classification of celiac disease based on the 4/5 rule

A
  • 1 Non classic CD
  • 2 Seronegative CD
  • 4 potential CD
  • 5 Non-responsive CD
175
Q

how many biopsied and where to take them in Celiac disease

A

at least 5 from duodenum and more then 1 from the duodenal bulb

176
Q

what is defined as gluten free?

A

< 20 part per million of gluten (20mg per kg of food)

177
Q

what can refractory celiac disease lead to?

A

ulcerative jejunitis

178
Q

what is acute diarrhea?

A

< 2 weeks but > 3 days and > 175-200g/day

179
Q

define chronic diarrhea

A

> 4w and > 200g/day or >= 3 stools/day

180
Q

causes of chronic diarrhea? (9)

A 
Chrons 
UC 
ischemic colitis 
colon cancer
radiation colitis 
pancreatic insufficiency 
bile acid deficiency 
SIBO 
SBS
181
Q

explain hydrogen malabsorption test?

A

nutrients are fermented by intestinal bacteria leading to increased H+, the level is measured every 30min over 3h (20ppm is the cutoff level)

For Fructose, lactose and glucose, SIBO

182
Q

anemia in Vit B12 malabsorption?

A

megaloblastic macrocytic anemia

large RBC and fragmented megaloblasts

183
Q

in shilling test how much B12 must be absorbed to have a normal uptake?

A

less then 7-10% meals malabsorption of B12

184
Q

Lactose intolerance due to?

A

lactase insufficiency causing bacteria to ferment lactose producing gass

185
Q

test in lactose intolerance?

A

H2 breath test + gene testing

186
Q

what would you recommend to a lactose intolerance patient?

A

no fermented dairy products
eat yoghurt and kefir
consider vit ADEK, B12 supplement

187
Q

Define intestinal failure?

A

when gut function is reduced to the point where IV nutrient supplementation is required to maintane health (IVS)

188
Q

etiology of intestinal failure?

A 
SBS 
intestinal fistulas 
dysmotility 
obstruction 
mucosal damage (IBD, cancer treatment)
189
Q

what is De Ritis ration?

A

De Ritis ratio is also known as Aspartate aminotransferase/alanine transaminase (AST/ALT) ratio

NORMAL VALUE 1.15

190
Q

which conditions showes a high De Ritis ratio?

A

Alcoholic liver disease
Organic toxic hepatitis
cirrhosis
intrahepatic cholestasis

191
Q

which conditions shows a low De Ritis ratio?

A

Acute viral hepatitis
Extrahepatic cholestasis
minor fatty liver disease

192
Q

treatment of H.pylori?

A

( ACCMMZ)

PPI
AC
MZ
CM

193
Q

medications given in nephrotic syndrom?

A

ACEI, ARBs
Statins
Anticoagulants
diuretics: spironolactone/thiazide

194
Q

What is SIADH and what are diseases associated with it

A

Increased ADH secretion (Fluid reabsorption)

seen in Pulmonary diseases and CNS diseases

195
Q

What is the volum status in a SIADH patient?

A

First water retention and overload, this then decreased aldosterone leading to Na excretion resulting in Euvolemic Hyponatremia and therfore cerebral edema.

196
Q

what are alarming symptoms where you don’t use the PPI for diagnosis GERD?

A 
dysphagia 
odynophagia 
GI bleeding 
anemia 
hematemesis 
weight loss
197
Q

Normal kidney size?

A

9-12 cm

4th year blocks (6 decks)

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