​Why is dapagliflizon help in IgA nephropathy ? 

• Reduces intraglomerular pressure (most important)

  • Increases sodium delivery to the macula densa.

  • Restores tubuloglomerular feedback, causing afferent arteriole vasoconstriction.

  • Lowers glomerular hyperfiltration and decreases ongoing glomerular injury.

• Reduces proteinuria

  • Less glomerular pressure → less protein leaks into the urine.

  • Proteinuria is a major predictor of CKD progression in IgA nephropathy.​

​

Type 1 Autoimmune Hepatitis Antibodies

• ANA (Antinuclear Antibodies): Targets components inside the nucleus of healthy cells.

• SMA / ASMA (Smooth Muscle Antibodies): Targets actin and other smooth muscle structural proteins.

• Anti-SLA/LP (Soluble Liver Antigen/Liver-Pancreas): Highly specific for AIH and often tested if ANA and SMA are negative. 

 

Type 2 Autoimmune Hepatitis Antibodies

• Anti-LKM-1 (Anti-Liver-Kidney Microsomal Type 1): Targets an enzyme inside liver and kidney cells (CYP2D6).

• Anti-LC-1 (Anti-Liver Cytosol Type 1): Targets formimidoyltransferase cyclodeaminase in the liver cell cytosol; sometimes found alongside anti-LKM-1.

​

What level of proteinuria defines nephrotic syndrome?

{{c1::Proteinuria >3.5 g/24 hours (3.5 g/day)}}

​

What are the indication of CABG? 

 

1. Left main disease: Blockage more than 50% in the main coronary artery 

2. Tripple vessel dsiease: narrowing in all 3 major heart arteries, with reduced heart function 

3. Left main equivalent: alot of blockages in both proximal LAD and circumflex arteries 

4. Multivessel disease with diabetes: alot of plaque buildup in patients who also have DM 

​

Here's the sequence:

1. Central sleep apnea → the brain temporarily stops sending respiratory drive to the diaphragm.

2. Apnea occurs → CO₂ rises and O₂ falls.

3. Once the CO₂ rises above the respiratory threshold, the brain overreacts and triggers hyperventilation.

4. The hyperventilation blows off too much CO₂, causing the CO₂ to fall below the apneic threshold.

5. Because the CO₂ is now too low, the brain stops breathing again → another central apnea.

6. This cycle repeats, producing the crescendo–decrescendo pattern of Cheyne–Stokes respiration.

​

What are the diagnostic criteria for acute liver failure (ALF)?

Back:
{{c1::No preexisting cirrhosis or chronic liver disease}}
{{c2::INR ≥1.5 (coagulopathy)}}
{{c3::Any degree of hepatic encephalopathy (altered mental status)}}
{{c4::Illness duration <26 weeks}}

NH3 is supposed the be converted into urea 

​

In acute liver failure (ALF), hepatic encephalopathy develops because the failing liver cannot adequately detoxify ammonia and other neurotoxins.

Mechanism

1. Hepatocyte failure → impaired conversion of ammonia (NH₃) to urea via the urea cycle.

2. Ammonia accumulates in the bloodstream.

3. Ammonia crosses the blood-brain barrier.

4. Astrocytes convert ammonia to glutamine, causing osmotic swelling of astrocytes.

5. This leads to cerebral edema, increased intracranial pressure, and hepatic encephalopathy.

​

Treatment for bile acid diarrhea (BAD) relies primarily on bile acid sequestrants like cholestyramine, colestipol, and colesevelam, alongside dietary fat reduction and treating any underlying conditions.  Cholestyramine: A powder packet mix (start at 4g daily) used as a first-line binder.Colestipol: Available in powder or easier-to-swallow tablets. Colesevelam: Tablet alternative that many patients find easier to tolerate.

​

What characteristic chest configuration is classically seen in patients with COPD (especially emphysema)?
Barrel chest

​

A patient with suspected choledocholithiasis should undergo direct ERCP if the total bilirubin is >{{c1::4.0 mg/dL}} and the common bile duct diameter is >{{c2::6 mm}} (with gallbladder in situ).​

​

Low EF → myocardial damage/remodeling Often due to prior MI or dilated cardiomyopathy.Damaged myocardium develops fibrosis and scar tissue.

Scar tissue → abnormal electrical conduction Creates areas where impulses can slow down and loop back (re-entry circuits). This predisposes to VT/VF. VT/VF → sudden cardiac death. The heart may suddenly stop pumping effectively.

​

What is the treatment of gastroparesis apart from metoclopramide?

{{c1::Erythromycin}}

 

Motilin Receptor Binding: It attaches to motilin receptors in the digestive tract, triggering strong stomach and upper gut contractions.

​

Then why NPO in pancreatitis because NPo wil decrease CCK hence less bile going to irriate the pancreas ?

If the patient eats: ↑ CCK↑ Pancreatic enzyme secretion ↑ Pancreatic exocrine activity

So keeping the patient NPO decreases CCK and secretin, allowing the pancreas to "rest" by reducing exocrine secretion.

​

​

When you eat, especially a fatty meal:

1. Fat enters the duodenum.

2. The duodenum releases cholecystokinin (CCK).

3. CCK causes the gallbladder to contract.

4. The gallbladder tries to squeeze bile through the blocked cystic duct.

5. This increases pain, inflammation, and intraluminal pressure.

So by keeping the patient NPO, you:

• ❌ Reduce CCK release.

• ❌ Prevent gallbladder contraction.

• ✅ Reduce pain and inflammation.

• ✅ Prepare the patient in case they need urgent surgery (laparoscopic cholecystectomy).

​

What type of viral esophageal ulcer is a punched-out ulcer?

 

{{c1::Herpes simplex virus (HSV) esophagitis}}

What type of viral esophageal ulcer is a linear (longitudinal) ulcer?

 

{{c2::Cytomegalovirus (CMV) esophagitis}}

How to treat ethylene glycol poisoning?

• Fompeziol (alcohol dehydrogenase inhibitor)

Which drugs does Augmentin contain?

• Amoxicillin and Clavulanic Acid

What are the 4 combinations of the drugs which include the peniccilin and the beta lactimase inhibtiros ?

- amoxicillin clavulanate ampicillin sulbactam and piperacillin tazobactam ticarcillin-clavulanate.

Penicillin Antibioticβ-Lactamase InhibitorCombination Name

--> AmoxicillinClavulanateAmoxicillin-clavulanate (Augmentin)

--> AmpicillinSulbactamAmpicillin-sulbactam (Unasyn)

--> PiperacillinTazobactamPiperacillin-tazobactam (Zosyn)

--> TicarcillinClavulanateTicarcillin-clavulanate (Timentin)

What is the prophylaxis for Tuberculosis?

• 9 months Isoniazid + Vitamin B6

• 4 Rafampin

• 3 Isonizaid + Rifampentin + Vitamin B6

What is the disease Lichen sclerosus? 

• Most commonly in post menopausal women, also present in the pubertal girl

• Common symptoms include intense pruritus, dyspareunia, and painful fissures.

What is Lichen Planus?

• Pruritic, Purple, Polygonal, Planar, Papules, and Plaques

Which disease is Lichen Planus associated with?

• Hepatitis C

What is Paget disease extramammary disease ?

• Paget disease extrammary disease is a rare, slow-growing cutaneous adenocarcinoma (skin cancer) that typically occurs in older adults, appearing as chronic, itchy, red-scaly plaques in apocrine gland-rich areas like the vulva, scrotum, perianal, or axillary regions.

A 2-week-old infant with bilious vomiting and refusal to feed. 

The parents report the baby hasbeen irritable and crying inconsolably, and occasionally lethargic. 

On physical examination, the abdomen is distended and tender, and bowel sound are decreased. 

Lab studies show metabolic acidosis (bowel ischemia → tissue hypoxia → lactic acidosis)  and imaging shows dilated loops of the small bowel. 

An upper GI series demonstrates a ''corkscrew" appearance of the duodenum. 

These findings indicate a surgical emergency requiring prompt intervention to prevent bowel necrosis. 

 

What is the likely diagnosis? 

​

Midgut volvulus

What happens to DLCO in asthma? 

​

Normal to increase 

​

The increase is mainly due to:

• Increased pulmonary capillary blood volume

• Intact alveolar membrane

​

Hence, it is a good exclusive criteria on USMLE questions. 

​

What happens to preload and afterload in HF ? 

Increase 

​

Alcohol Withdrawal symptoms:

3–36h → GI upset Agitation Insomnia Tremor

6–48h → Seizures

12–48h → Hallucinosis

48–96h → DTs

​

​

What is the underlying cause of Transient Tachypnea of the Newborn (TTN)?

Delayed clearance of fetal lung fluid

​

What is the classic CXR finding in Transient Tachypnea of the Newborn?

Prominent interlobar fissures with pulmonary edema (fluid in fissures)

​

​

What is the underlying cause of Neonatal Respiratory Distress Syndrome (NRDS)?

Surfactant deficiency due to immature type II pneumocytes

What is the pathophysiology of NRDS?
↓ Surfactant → ↑ alveolar surface tension → alveolar collapse (atelectasis)

What L/S ratio in amniotic fluid indicates adequate fetal lung maturity?
≥ 2

What L/S ratio predicts NRDS?
< 1.5

• Lecithin (phosphatidylcholine) is the main component of pulmonary surfactant.

• Lecithin (surfactant component)

• Sphingomyelin (remains relatively constant)

​

What cancer risk increases with combined estrogen-progestin HRT?
Breast cancer

​

Which antiviral drug is associated with Cushing syndrome?

 

Ritonavir

• Protease inhibitor

• Strong CYP3A4 inhibitor

• ↑ Steroid levels when combined with glucocorticoids

• → Iatrogenic Cushing syndrome

💡 Think: Ritonavir = drug interaction Cushing

Which antiviral drug is associated with bone marrow suppression?

 

Zidovudine

• NRTI

• Major toxicity: bone marrow suppression

  • Macrocytic anemia

  • Neutropenia

What is something common between Gilbert syndrome and Crigler-Najjar syndrome?

- Both cause unconjugated hyperbilirubinemia due to impaired bilirubin conjugation.

 

What enzyme is deficient in Crigler-Najjar syndrome?

- UDP-glucuronyl transferase (UGT1A1)

 

What is the difference between Crigler-Najjar syndrome Type 1 and Type 2?

Type 1:

- Complete absence of UDP-glucuronyl transferase → severe unconjugated hyperbilirubinemia

Type 2:

- Partial deficiency of UDP-glucuronyl transferase → milder disease

UDP-glucuronyl transferase (UGT1A1)

​

​

What are the causes of avascular necrosis of the bone?​

CASTS Bend LEGS 

Corticosteriods 

Alcohol 

Sickle cell disease 

Trauma 

SLE

 

Bends disease 

 

Legg-Calve-Perthes disease 

Gaucher 

SCFE 

 

 

What is the definition of Avascular necrosis of the bone? 

- Infraction of the bone and marrow is usually very painful. 

​

What does DRESS stand for?
- Drug Reaction with Eosinophilia and Systemic Symptoms.

What is DRESS Syndrome?

DRESS syndrome is a severe, potentially life-threatening delayed hypersensitivity drug reaction characterized by:

• Diffuse rash

• Fever

• Lymphadenopathy

• Eosinophilia

• Multiorgan involvement (most commonly liver, but can also affect kidneys, lungs, and heart)

Symptoms usually occur 2–8 weeks after starting the offending drug, which is a classic USMLE test clue.

Common Causes of DRESS Syndrome

High-yield drugs include:

• Anticonvulsants

  • Phenytoin

  • Carbamazepine

• Antibiotics

  • Vancomycin

  • Sulfonamides

• Other drugs

  • Allopurinol

​​

Light's criteria

 

A pleural effusion is exudative if ANY ONE of these is true:

 

1. Protein ration

- Pleural fluid protein/ Serum Protein > 0.5

2. LDH ratio

- Pleural fluid LDH/ Serum LDH > 0.6

3. Absolute LDH

- Pleural fluid LDH > 2/3 of the upper limit of normal serum LDH

​

What does the 2 As in the MONA BASCH mnemonic stand for ? ​

​

Aspirin and Ace inhibitors 

​

​

What is the formula of the ejection fraction ? 

 

SV/EDV

 

What is the normal range of ejection fraction ?

 

50% to 70%

​

What is the MOA of hydralazine ? 

cGMPŽsmooth muscle relaxation. Hydralazine vasodilates arterioles > veins; afterload reduction.

​

​

Where does the thoracic duct drain?
Drains most of the body → into the left internal jugular vein + left subclavian vein (left venous angle)

Where does the right lymphatic duct drain?
Drains right upper quadrant only (right head/neck, right arm, right thorax) → into the right internal jugular vein + right subclavian vein (right venous angle)

​​

​

• Distal radius fracture with dorsal displacement (extension): Colles fracture

• Distal radius fracture with volar displacement (flexion): Smith fracture

​

MEHLMAN Q#1556

​​

Long term use of steriods cause ?

- Long term use of steriods cause --> Adicoyte hypertrophy, left hip pain 

​

What is the intubation criteria?

GCS less than 8 

Ph less than 7.25 

Sp O2 less than 90 percent 

​

After which procedures shall we do infective endocarditis prophylaxis ? 

 

RASG
Resp mucosal incision —> Amox
Apical tooth manipulation —> Amox
Surgery on infected skin or muscle —> Vanc
GI or GU procedure  active infection —> Ampi

Which structure is responsible for allowing the passages of air, fluid, phagocytes, and bacteria between alveoli ? 

• Pores of kohn

What is a colombo eye ? 

- Gap of the iris 

What is the cause of the increase PSA ? ​

BPH or PC

​

correct = PC 

• BPH → PSA rises because of increased mass

• Prostate cancer → PSA rises because of leakage + abnormal tissue

​

Heart failure with reduced ejection fraction is below:
≤40%

​

HFmrEF (mid-range / mildly reduced EF)
41–49%

​

Heart failure with preserved ejection fraction is above:
≥50%

​​

​

What is the definitive treatment of constrictive pericarditis?

Pericardiectomy

 

A pericardiectomy (surgical removal of the pericardium) is the definitive treatment because it:
Removes the constricting layer
Allows the ventricles to expand normally during diastole
Improves cardiac filling and output
So yes — you can think of it as relieving the external pressure on the heart, but more specifically:
It removes the noncompliant pericardial constraint that is impairing ventricular filling.

​

Foreman Ceacum which means blind 

• Cecum (intestine) = blind pouch  (A blind-ended pouch at the beginning of the large intestine and Where the small intestine empties into the colon) 

• Foramen cecum (tongue) = blind hole

​

In the tongue, the foramen cecum:

• Is a small pit/depression at the base of the tongue

• Marks the origin of the thyroglossal duct

👉 It’s called “cecum” here because it’s a blind pit, not because it’s related to the intestine.

​

What happens to hepcidin in hemochromatosis ? 

-

Hemochromatosis = ↓ hepcidin → ↑ ferroportin activity → ↑ intestinal iron absorption → iron overload → ↑ ferritin

 

What hepcidin normally does:

Made by the liver

Blocks iron absorption by degrading ferroportin (the iron exporter)

So:

↑ Hepcidin → ↓ iron absorption

↓ Hepcidin → ↑ iron absorption

​

Why Hepcidin is decreased in hemochromatosis? 

• Pathogens (bacteria) need iron to grow

• So the body “hides” iron to starve them
  → this is called nutritional immunity

​

What is the MOA of Fibrates ?

​

Activate PPAR-α —>  􏰁upregulate LPL􏰁􏰀 —> TG clearance
Activate PPAR- a —> 􏰁induce HDL synthesis

​

LPL —> Glycerol 3 P and FFA  converts into TG 

Lipoprotein lipase effect:

It decreases triglycerides (TG) in the blood.

Why?

It breaks them down:

TG → Free fatty acids (FFA) + glycerol
What happens next:
FFA → taken up by muscle (energy) or adipose (storage)
Glycerol → goes to liver

​

What is the MOA of Bile acid resins ? 

​

Disrupt enterohepatic bile acid circulation 􏰁  —> compensatory 􏰀increase conversion of cholesterol
to bile —> decrease 􏰁􏰂intrahepatic cholesterol􏰁􏰀 —> increase LDL receptor recycling

Bile acid resins (like cholestyramine, colestipol, colesevelam) work by binding bile acids in the intestine and preventing their reabsorption. Here’s what happens downstream:

Bile acid loss – Because they are excreted in the stool instead of being recycled, the liver needs to make more bile acids.
Increased cholesterol use – To make more bile acids, the liver pulls cholesterol from the blood. This lowers LDL cholesterol in the blood.
Effect on bile composition – The liver converts cholesterol into bile acids, so the bile actually becomes richer in bile acids, not cholesterol itself. However, because cholesterol is being pulled out of the blood to make bile acids, the total cholesterol in bile may actually slightly increase in some contexts, but this is not the primary effect.

​

What is the MOA  of NIACN ?
 

Inhibits lipolysis (hormone- sensitive lipase) in adipose tissue; reduces hepatic VLDL synthesis

HSL breaks down TG which 
releases FFA and glycerol into the blood  

​

​

What is first-line antiviral treatment for chronic Hepatitis B?

 

Tenofovir or Entecavir

​

Tenofovir is a nucleotide reverse transcriptase inhibitor (NRTI) that works by inhibiting viral replication in HIV-1 and Hepatitis B (HBV). After conversion to its active form, tenofovir diphosphate, it competes with natural substrates for viral DNA polymerase, causing chain termination and halting DNA synthesis. 

 

Entecavir is a potent guanosine nucleoside analogue used to treat chronic Hepatitis B (HBV) by inhibiting the HBV polymerase enzyme. It works by being phosphorylated to its active triphosphate form, which acts as a competitor to natural dGTP, inhibiting three key steps in viral DNA synthesis: base priming, reverse transcription, and positive strand DNA synthesis. 

​

Asthma first line ?
--> Low ICS + Fomoterol  

​

​

First line COPD tx?  = 

--> First line is LABA or LAMA and then escalate 
--> Directly to dual therapy LABA + LAMA 

​

​

What is the cardinal symptoms of COPD exacerbation ? 

• Increased Dyspnea (Shortness of Breath): Feeling more breathless than usual, even with routine daily activities like showering, walking, or talking.

• Increased Sputum Volume: Producing a significantly larger amount of mucus (phlegm) than the daily baseline.

• Increased Sputum Purulence: A change in the color of mucus from clear/white to dark yellow, green, or brown, indicating increased inflammation.

​

Heparin induced thrombocytopenia type 1 what will be the platelets levels ?

​

Above 100,000 cells per microliter 

​

​

why melena occurs in upper gi bleed?

• Blood from an upper GI source (esophagus, stomach, duodenum) travels through the GI tract

• It gets exposed to:

  • Gastric acid

  • Digestive enzymes (especially proteases)

  • Intestinal bacteria

Key mechanism:

• Hemoglobin is broken down into hematin (and other iron-containing compounds)

• This gives stool the black, tarry appearance and characteristic smell

Role of acid vs oxidation:

• ✅ Acid & enzymes → PRIMARY cause (digestion of blood)

• ✅ Bacterial degradation → contributes

• ⚠️ Oxidation → minor role, not the main explanation

High-yield way to remember:

Melena = digested blood

Extra exam pearls:

• Usually requires ~50–100 mL of blood in upper GI tract

• Slow bleeding → more time for digestion → melena

• Rapid/heavy bleeding → may present as hematochezia instead

Which bilirubin is water soluble ? 
Conjugated bilirubin 

​

Which bilirubin fat soluble ?

unconjugated bilirubin 

​

What skin manifestation of liver cirrhosis with high estrogen ? 
Spider angioma and palmar erythema 

​

What VHL ?

​

RCC 

Hemangioblastoma 

lots of catecholamines 

​

​What are the drug causes of hyper kalemia 

​

D
S

HCT

​

​

​

​Hyposomoalirty causes hypokalemia --> Shift of water into cells 
causes shift of K+ into cells 

 

​What is the criteria for diagnosis of orthostatic hypotension? {{c1::drop of SBP more than 20 and drop of DBP more than 10 mmHg and the a raise of HR more than 10 bpm }} When do we do hemodialysis ? {{c2::ECG changes or ventricular arrythmias}} In what ingestions do we do hemodialysis ? {{c3:: Sodium valproate }} {{c4:: Salicylates }} {{c5:: Carbamazepine }} {{c6::Lithium}} {{c7::Toxic Alcohol (methanol, ethylene glycogl }} When do we use hemodialysis ? {{c8::Encphalitis }} {{c9::Bleeding}} {{c10::pericarditis }}

​​

1. G6PD deficiency → oxidative damage

• Problem: ↓ NADPH → ↓ glutathione

• Result: RBCs can’t handle oxidative stress

• Leads to:

  • Hemoglobin denaturation (Heinz bodies)

  • Membrane damage → hemolysis

2. Pyruvate kinase deficiency → ↓ ATP

• In Pyruvate kinase deficiency:

  • ↓ ATP → Na⁺/K⁺ ATPase fails 

  • Na⁺ accumulates inside → water balance gets disrupted

  • RBC becomes dehydrated and rigid

  ❌ No toxic metabolite buildup here—just energy failure

​

​

What is the treatment of calcium oxalate

stones ?

 

{{c1::Thaizide}} 

 

{{c2::Citrate}} 

 

low {{c3::sodium diet }}

 

How Low Citrate Leads to Stones:
Reduced Calcium Binding (Complexation): Citrate normally binds to calcium in the urine, forming a soluble complex (\(Ca-Cit\)). This reduces the amount of free (ionic) calcium available to bind with oxalate or phosphate, which are the main components of kidney stones.

 

Increased Renal Reabsorption: Thiazides inhibit the \(NaCl\) transporter (NCC) in the DCT. This decreases sodium levels inside the cell, strengthening the gradient for the sodium-calcium exchanger, which pulls calcium into the bloodstream.

 

 

A low-sodium diet helps prevent calcium kidney stones because high salt intake causes the kidneys to excrete more calcium into the urine (hypercalciuria), which then forms stones. Reducing sodium helps decrease this urinary calcium leakage, limiting the amount of calcium available to combine with other substances like oxalate to create stones.

​

​

What is the cystinruia ?

{{c2::PCT reabsorption defect of OLA aminoacid }}

 

What is the tx of cystinuria ?

 

{{c1::penicillamine}}

penicillamine are used to bind to cystine, creating a more soluble complex.

​

What is the cause of IDA ?

Colon cancer 

Microcytic anemia with normal ferritin and TIBC → next step?

Hemoglobin electrophoresis

​

Causes of b12 defiency 

--> Crohn disease 

--> pernicious disease  

--> Bypass 

 

 

What is the dietary source of folate ? 

 

Leafy green 

 

What is the dietary source of B12 ?

 

Animal products 

​

What is the underlying problem in sideroblastic anemia?
 

alcohol, MDS, X linked, Defective heme synthesis → iron trapped in mitochondria, Isoniazid, linezolid Copper, isoniazid, lead and vitamin b6 

How to tell the differenece between b12 and b9 defeincy ? 

 

Increase MMA in b12 deficiency 

​

What are the signs of the hemolytic anemia ? 

PUURL  H 

Pigmented Gallstones 
Urobilinogen 
Unconjugated bilirubin 
Reticulocytes 
LDH 

Haptoglobin (decreased)

​

Pigmented gallstones (specifically black pigment stones) are a common complication of hemolysis because the accelerated breakdown of red blood cells leads to an excess of bilirubin in the bile, which precipitates as insoluble calcium bilirubinate. 

Medscape +1

Here is the step-by-step mechanism of why this occurs:

• Excess Bilirubin Production: Hemolysis (destruction of red blood cells), found in conditions like sickle cell anemia or hereditary spherocytosis, releases large amounts of hemoglobin.

• Increased Conjugation and Secretion: The liver breaks down this excess hemoglobin into bilirubin, increasing the total amount of bilirubin that is conjugated and excreted into the bile.

​

What are common triggers of sickle cell crisis?
{{c1::Hypoxia, dehydration, acidosis 

(also infection, cold, high altitude)}}

 

 

What is the acute treatment of sickle cell crisis?

{{c1::Hydration, oxygen, pain control (opioids), ± transfusion}}

 

What is the chronic treatment of sickle cell disease?
{{c2::Hydroxyurea (↑ HbF), ± chronic transfusions}}

 

What are the common triggers of G6PD ?

{{c3::Dapsone}} 

{{c4::Nitrofuratonin}} 

 

What is the best test to diagnose HS ?

{{c5::Osmotic fragility }}

 

Cold AIHA is associated with IgM 

Warm AIHA is associated with IgG

 

How to diagnoe PNH ? 

{{c6::

 

Flow cytometery  

}}

 

How to tx PNH ? 

 

{{c7::

Eculizumab

}}

 

Tx of AML M3 ?
{{c8::Vit A}}

 

Tx of CML ?

 {{c9::Imatanib}}

​

So in VWF disease factor 8 is decrease because there is low amount of production of factor 8 by the platelets ?

What actually happens

vWF has two key roles:

Helps platelet adhesion

Stabilizes and protects factor VIII in circulation

 

👉 So in von Willebrand disease:

 

↓ vWF → factor VIII gets degraded faster

Result → secondary decrease in factor VIII levels

🧠 Simple way to remember

vWF = “carrier + protector” of factor VIII

No vWF → factor VIII becomes unstable and breaks down

​

​

What is the treatment of latent tb ? {{c1:: Rifapentine (RPT) and Isoniazid (INH): Weekly for 3 months (12 doses).}} {{c2::Rifampin (RIF): Daily for 4 months.}} {{c3::Isoniazid (INH) and Rifampin (RIF): Daily for 3 months.}} Is this a good flash card ?

​

​

> 5 mm 

 

{{c2::Close contacts }}

{{c1::HIV AIDS }}

 

> 10 mm 

 

{{c3::Homless }}

{{c4::travelers }}

{{c5::prisoners}} 

​

​

Target MAP in septic shock?
→ {{c1::≥ 65 mmHg}}

 

Target urine output in shock?
→ {{c2::≥ 0.5 mL/kg/hr}}

 

 

• What was included in early goal-directed therapy?
  → {{c3::CVP, ScvO₂ monitoring (now less emphasized)}}

​What disease is caused by C1 esterase inhibitor deficiency?
{{c1::Hereditary angioedema}}

​​

​

which artery is ruptured in epidural hematoma ?

e rupture of the middle meningeal artery

 

​

The middle meningeal artery runs:

 

between the skull and the dura mater

in grooves on the inner surface of the temporal/parietal bonesThe middle meningeal artery is primarily a branch of the maxillary artery, which is itself one of the terminal branches of the external carotid artery.

 

H. pylori infection → Chronic gastritis → Atrophic gastritis → Intestinal metaplasia → Dysplasia → Intestinal-type gastric adenocarcinoma
CDH1 (E-cadherin) mutation → Loss of cellular adhesion → Signet ring cells infiltrate gastric wall → Diffuse-type gastric adenocarcinoma
Normal gastric epithelium (simple columnar mucus-secreting cells) → Intestinal-type epithelium with goblet cells

​

Extra-adrenal pheochromocytoma = 

​

{{c1::Paraganglioma.}}

​

What is the probability of fat emoblism syndrome in a single long bone ? 

​

The probability of fat embolism syndrome (FES) with a single long bone fracture is 1-3%; this increases to 33% with bilateral femur fractures.

​

Apoplexy Apo means Plexy = growth

apo- = away from, off, or down

-plexy (from plēxis) = a strike, blow, or smiting

So apoplexy literally means "struck down by a blow."

 

Pituitary apoplexy – sudden hemorrhage or infarction of the pituitary gland.

​

What test determines good chest compressions?

{{c1::Capnography (end-tidal CO₂, EtCO₂ monitoring)}}

​

​"CO₂ follows blood flow." The more blood your chest compressions move to the lungs, the more CO₂ is exhaled, and the higher the EtCO₂ reading.

​

​What is the MOA of calcitonin ? 

1. Effect on Bones (Antiresorptive Action)

• Inhibits Osteoclasts: Calcitonin binds directly to specific G-protein coupled receptors on osteoclasts (the cells responsible for bone resorption). [1, 2]

• Reduces Bone Breakdown: This binding causes an increase in intracellular cAMP, which rapidly halts the ability of osteoclasts to break down bone and release calcium into the bloodstream. [1, 2]

• Decreases Bone Turnover: By reducing osteoclast activity and motility, calcitonin slows the overall rate of bone turnover, helping to preserve bone mass and strength in conditions like osteoporosis.

​

Why does immbolizaiton cause hypercalcemia ? 

• Normal bone remodeling

  • Bones are constantly remodeled by:

    • Osteoclasts → break down bone and release calcium into the blood.

    • Osteoblasts → build new bone.

• Mechanical loading normally stimulates osteoblasts

  • Weight-bearing activity and muscle contractions signal osteoblasts to form bone.

  • This keeps bone formation and resorption balanced.

• With immobilization

  • There is loss of mechanical stress on bone.

  • Osteoblast activity decreases (less bone formation).

  • Osteoclast activity initially remains relatively increased or becomes dominant, leading to increased bone resorption.

What is the second-line pharmacologic treatment for neuroleptic malignant syndrome (NMS)?
{{c1::Dantrolene}}

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What is the mechanism of action of dantrolene?

{{c2::**Blocks the ryanodine receptor (RyR1) in skeletal muscle, reducing calcium release from the sarcoplasmic reticulum and decreasing muscle contraction.}}

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How does Adenosine cause vasodilation ? 

1. Adenosine binds to A₂ receptors (especially A₂A receptors) on vascular smooth muscle cells.

2. These receptors are Gs protein-coupled receptors, so they activate adenylyl cyclase.

3. Adenylyl cyclase increases cAMP inside the cell.

4. Increased cAMP activates protein kinase pathways that:

   • reduce intracellular calcium

   • inhibit myosin light-chain kinase

5. Less calcium + less MLCK activity → smooth muscle relaxes.

6. Relaxed smooth muscle = vasodilation. 

How does adenosine cause bronchoconstirction ?

• Adenosine binds to A₃ receptors on mast cells in the airway.

• This causes mast cell degranulation.

• Mast cells release inflammatory mediators:

  • Histamine

  • Leukotrienes

  • Prostaglandins

• These mediators cause:

  • Bronchial smooth muscle contraction

  • Airway mucus secretion

  • Airway inflammation

• Result → bronchoconstriction/bronchospasm

 

 

 

 

 

 

 

 

 

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