High-Yield USMLE Steps Cards
@highyield-usmle.bsky.social
Methimazol & Propylthiouracil
-↓Thyroid hormones via THYROID PEROXIDASE, enzyme responsible for both IODINE ORGANIFICATION & COUPLING OF IODOTYROSINES.
Propylthiouracil also decreases the peripheral conversion of T4 to T3.
-↓Thyroid hormones via THYROID PEROXIDASE, enzyme responsible for both IODINE ORGANIFICATION & COUPLING OF IODOTYROSINES.
Propylthiouracil also decreases the peripheral conversion of T4 to T3.
July 20, 2025 at 5:28 PM
Methimazol & Propylthiouracil
-↓Thyroid hormones via THYROID PEROXIDASE, enzyme responsible for both IODINE ORGANIFICATION & COUPLING OF IODOTYROSINES.
Propylthiouracil also decreases the peripheral conversion of T4 to T3.
-↓Thyroid hormones via THYROID PEROXIDASE, enzyme responsible for both IODINE ORGANIFICATION & COUPLING OF IODOTYROSINES.
Propylthiouracil also decreases the peripheral conversion of T4 to T3.
Hyperthyroidism causes:
-↓Systemic vascular resistance
-↓Diastolic pressure
-↑Systolic pressure
-↑Pulse pressure
-High-output heart failure
Also:
-Tachycardia/palpitations
-Atrial fibrillation
-↑Pulmonary artery pressure
-↑EF & CO
-Myocardial oxygen demand & angina
-↓Systemic vascular resistance
-↓Diastolic pressure
-↑Systolic pressure
-↑Pulse pressure
-High-output heart failure
Also:
-Tachycardia/palpitations
-Atrial fibrillation
-↑Pulmonary artery pressure
-↑EF & CO
-Myocardial oxygen demand & angina
July 20, 2025 at 5:24 PM
Hyperthyroidism causes:
-↓Systemic vascular resistance
-↓Diastolic pressure
-↑Systolic pressure
-↑Pulse pressure
-High-output heart failure
Also:
-Tachycardia/palpitations
-Atrial fibrillation
-↑Pulmonary artery pressure
-↑EF & CO
-Myocardial oxygen demand & angina
-↓Systemic vascular resistance
-↓Diastolic pressure
-↑Systolic pressure
-↑Pulse pressure
-High-output heart failure
Also:
-Tachycardia/palpitations
-Atrial fibrillation
-↑Pulmonary artery pressure
-↑EF & CO
-Myocardial oxygen demand & angina
Autoimmune gastritis (against parietal cell)
-↓Parietal cell mass
-↓Gastric acid→↑Gastrin release by antral G cells→↑Gastric pH
-↓Intrinsic factor production
-Vit B12 deficiency (megaloblastic anemia, subacute combined degeneration
B cells autoantibodies against
-H/K-ATPase
-Intrinsic factor
-↓Parietal cell mass
-↓Gastric acid→↑Gastrin release by antral G cells→↑Gastric pH
-↓Intrinsic factor production
-Vit B12 deficiency (megaloblastic anemia, subacute combined degeneration
B cells autoantibodies against
-H/K-ATPase
-Intrinsic factor
July 20, 2025 at 5:11 PM
Autoimmune gastritis (against parietal cell)
-↓Parietal cell mass
-↓Gastric acid→↑Gastrin release by antral G cells→↑Gastric pH
-↓Intrinsic factor production
-Vit B12 deficiency (megaloblastic anemia, subacute combined degeneration
B cells autoantibodies against
-H/K-ATPase
-Intrinsic factor
-↓Parietal cell mass
-↓Gastric acid→↑Gastrin release by antral G cells→↑Gastric pH
-↓Intrinsic factor production
-Vit B12 deficiency (megaloblastic anemia, subacute combined degeneration
B cells autoantibodies against
-H/K-ATPase
-Intrinsic factor
Myelination= ↑length constant, ↓time constant
Demyelination= ↓length constant, ↑time constant
Demyelination= ↓length constant, ↑time constant
July 20, 2025 at 5:04 PM
Myelination= ↑length constant, ↓time constant
Demyelination= ↓length constant, ↑time constant
Demyelination= ↓length constant, ↑time constant
HIGH-ALTITUDE
-Hypoxemia (↓O2, normal 75-100 mmHg)
-Hyperventilation (↓PaCO2, normal 35-45 mmHg)→ respiratory alkalosis
-↑HCO3 excretion (to compensate alkalosis) <24 mEq/L
-Hypoxemia (↓O2, normal 75-100 mmHg)
-Hyperventilation (↓PaCO2, normal 35-45 mmHg)→ respiratory alkalosis
-↑HCO3 excretion (to compensate alkalosis) <24 mEq/L
July 20, 2025 at 4:52 PM
HIGH-ALTITUDE
-Hypoxemia (↓O2, normal 75-100 mmHg)
-Hyperventilation (↓PaCO2, normal 35-45 mmHg)→ respiratory alkalosis
-↑HCO3 excretion (to compensate alkalosis) <24 mEq/L
-Hypoxemia (↓O2, normal 75-100 mmHg)
-Hyperventilation (↓PaCO2, normal 35-45 mmHg)→ respiratory alkalosis
-↑HCO3 excretion (to compensate alkalosis) <24 mEq/L
Normal aging respiratory system:
-↑V/Q mismatch (due to basilar microatelectasis causing shunt effect)
-↑Dead space (loss of alveolar surface area)
-↑A(lveolar)-a(rterial) oxygen gradient → ↓PaO2 w/NO hypoventilation (ie normal PaCO2)
-↑V/Q mismatch (due to basilar microatelectasis causing shunt effect)
-↑Dead space (loss of alveolar surface area)
-↑A(lveolar)-a(rterial) oxygen gradient → ↓PaO2 w/NO hypoventilation (ie normal PaCO2)
July 20, 2025 at 4:45 PM
Normal aging respiratory system:
-↑V/Q mismatch (due to basilar microatelectasis causing shunt effect)
-↑Dead space (loss of alveolar surface area)
-↑A(lveolar)-a(rterial) oxygen gradient → ↓PaO2 w/NO hypoventilation (ie normal PaCO2)
-↑V/Q mismatch (due to basilar microatelectasis causing shunt effect)
-↑Dead space (loss of alveolar surface area)
-↑A(lveolar)-a(rterial) oxygen gradient → ↓PaO2 w/NO hypoventilation (ie normal PaCO2)
HEPCIDIN
-Inflammatory cytokine (chronic diseases)
-↓Iron absorption
-↓Iron release from the reticuloendothelial system
By inactivating iron channels on enterocytes & reticuloendothelial macrophages
Net result:
-Normo/microcytic anemia w/low reticulocyte responde
-↓Serum iron
-↔︎/↓total iron binding
-Inflammatory cytokine (chronic diseases)
-↓Iron absorption
-↓Iron release from the reticuloendothelial system
By inactivating iron channels on enterocytes & reticuloendothelial macrophages
Net result:
-Normo/microcytic anemia w/low reticulocyte responde
-↓Serum iron
-↔︎/↓total iron binding
July 20, 2025 at 4:40 PM
HEPCIDIN
-Inflammatory cytokine (chronic diseases)
-↓Iron absorption
-↓Iron release from the reticuloendothelial system
By inactivating iron channels on enterocytes & reticuloendothelial macrophages
Net result:
-Normo/microcytic anemia w/low reticulocyte responde
-↓Serum iron
-↔︎/↓total iron binding
-Inflammatory cytokine (chronic diseases)
-↓Iron absorption
-↓Iron release from the reticuloendothelial system
By inactivating iron channels on enterocytes & reticuloendothelial macrophages
Net result:
-Normo/microcytic anemia w/low reticulocyte responde
-↓Serum iron
-↔︎/↓total iron binding
Heparin binds indirectly to antithrombin III, which neutralizes factor Xa & thrombin.
-↓Factor Xa
-Prolonged PTT/TT
Dabigatran directly inhibits thrombin
RivaroXaban inhibits factor Xa
-↓Factor Xa
-Prolonged PTT/TT
Dabigatran directly inhibits thrombin
RivaroXaban inhibits factor Xa
July 20, 2025 at 4:14 PM
Heparin binds indirectly to antithrombin III, which neutralizes factor Xa & thrombin.
-↓Factor Xa
-Prolonged PTT/TT
Dabigatran directly inhibits thrombin
RivaroXaban inhibits factor Xa
-↓Factor Xa
-Prolonged PTT/TT
Dabigatran directly inhibits thrombin
RivaroXaban inhibits factor Xa
Hartnup disease (niacin deficiency)
-Neutral amino acids in urine
-Pellagra-like skin eruptions
-Cerebellar ataxia
Caused by impaired transport of neutral amino acids in the small intestine and proximal tubule of the kidney.
-Neutral amino acids in urine
-Pellagra-like skin eruptions
-Cerebellar ataxia
Caused by impaired transport of neutral amino acids in the small intestine and proximal tubule of the kidney.
July 17, 2025 at 7:28 PM
Hartnup disease (niacin deficiency)
-Neutral amino acids in urine
-Pellagra-like skin eruptions
-Cerebellar ataxia
Caused by impaired transport of neutral amino acids in the small intestine and proximal tubule of the kidney.
-Neutral amino acids in urine
-Pellagra-like skin eruptions
-Cerebellar ataxia
Caused by impaired transport of neutral amino acids in the small intestine and proximal tubule of the kidney.
Peritubular fibroblast cells in the renal cortex: erythropoietin
Juxtaglomerular cells in the distal tubule: renin
Juxtaglomerular cells in the distal tubule: renin
July 17, 2025 at 7:16 PM
Peritubular fibroblast cells in the renal cortex: erythropoietin
Juxtaglomerular cells in the distal tubule: renin
Juxtaglomerular cells in the distal tubule: renin
Duchenne muscular dystrophy
-X-linked recessive myopathy
-Frameshift deletions affecting the dystrophin gene
-Mutation affects the sarcolemma cytoskeleton linker protein (loses the stabilization interaction between the sarcolemma and the intracellular contraction apparatus)
-X-linked recessive myopathy
-Frameshift deletions affecting the dystrophin gene
-Mutation affects the sarcolemma cytoskeleton linker protein (loses the stabilization interaction between the sarcolemma and the intracellular contraction apparatus)
July 17, 2025 at 2:23 PM
Duchenne muscular dystrophy
-X-linked recessive myopathy
-Frameshift deletions affecting the dystrophin gene
-Mutation affects the sarcolemma cytoskeleton linker protein (loses the stabilization interaction between the sarcolemma and the intracellular contraction apparatus)
-X-linked recessive myopathy
-Frameshift deletions affecting the dystrophin gene
-Mutation affects the sarcolemma cytoskeleton linker protein (loses the stabilization interaction between the sarcolemma and the intracellular contraction apparatus)
Hyperparathyroidism causes ↑RANK-L expression and ↓OPG expression, leading to net bone loss.
Expression of RANK-L on osteoblasts induces ↑bone resorption via a paracrine effect on nearby osteoclasts.
Expression of RANK-L on osteoblasts induces ↑bone resorption via a paracrine effect on nearby osteoclasts.
July 17, 2025 at 2:17 PM
Hyperparathyroidism causes ↑RANK-L expression and ↓OPG expression, leading to net bone loss.
Expression of RANK-L on osteoblasts induces ↑bone resorption via a paracrine effect on nearby osteoclasts.
Expression of RANK-L on osteoblasts induces ↑bone resorption via a paracrine effect on nearby osteoclasts.
Aminoglycosides (gentamicin) inhibit mRNA genetic code reading & protein synthesis by binding to the prokaryotic 30S ribosomal subunit.
July 17, 2025 at 1:57 PM
Aminoglycosides (gentamicin) inhibit mRNA genetic code reading & protein synthesis by binding to the prokaryotic 30S ribosomal subunit.
VWF disease (AD)
-Normal platelets
-Normal PT
-Prolonged PTT (due to low levels of factor VIII, bc VWF is the carrier protein & protects it from degradation).
-Normal platelets
-Normal PT
-Prolonged PTT (due to low levels of factor VIII, bc VWF is the carrier protein & protects it from degradation).
July 17, 2025 at 1:52 PM
VWF disease (AD)
-Normal platelets
-Normal PT
-Prolonged PTT (due to low levels of factor VIII, bc VWF is the carrier protein & protects it from degradation).
-Normal platelets
-Normal PT
-Prolonged PTT (due to low levels of factor VIII, bc VWF is the carrier protein & protects it from degradation).
De Quervain tendinopathy is characterized by tendinous myxoid degeneration and thickening of tendon sheats involving the ABDUCTOR POLLICIS LONGUS and EXTENSOR POLLICIS BREVIS in the first extensor compartment.
July 16, 2025 at 11:35 PM
De Quervain tendinopathy is characterized by tendinous myxoid degeneration and thickening of tendon sheats involving the ABDUCTOR POLLICIS LONGUS and EXTENSOR POLLICIS BREVIS in the first extensor compartment.
SLE antibodies
-Sensitive: ANAs
-Specific: Ant-dsDNA & anti-Smith
-Sensitive: ANAs
-Specific: Ant-dsDNA & anti-Smith
July 16, 2025 at 11:28 PM
SLE antibodies
-Sensitive: ANAs
-Specific: Ant-dsDNA & anti-Smith
-Sensitive: ANAs
-Specific: Ant-dsDNA & anti-Smith
Vitamin B12 deficiency
-Megaloblastic anemia (impaired DNA synthesis)
-Neurologic deficits (impaired myelin synthesis)
-Subacute combined degeneration of the dorsal columns & lateral corticospinal cord.
Elevations in:
-Methylmalonic acid
-Homocysteine
Due to decreased metabolism of these molecules.
-Megaloblastic anemia (impaired DNA synthesis)
-Neurologic deficits (impaired myelin synthesis)
-Subacute combined degeneration of the dorsal columns & lateral corticospinal cord.
Elevations in:
-Methylmalonic acid
-Homocysteine
Due to decreased metabolism of these molecules.
July 16, 2025 at 11:27 PM
Vitamin B12 deficiency
-Megaloblastic anemia (impaired DNA synthesis)
-Neurologic deficits (impaired myelin synthesis)
-Subacute combined degeneration of the dorsal columns & lateral corticospinal cord.
Elevations in:
-Methylmalonic acid
-Homocysteine
Due to decreased metabolism of these molecules.
-Megaloblastic anemia (impaired DNA synthesis)
-Neurologic deficits (impaired myelin synthesis)
-Subacute combined degeneration of the dorsal columns & lateral corticospinal cord.
Elevations in:
-Methylmalonic acid
-Homocysteine
Due to decreased metabolism of these molecules.
Insulin upregulates LIPOPROTEIN LIPASE, which hydrolyzes triglycerides in chylomicrons and VLDL; the liberated fatty acids are largely taken up and esterified in adipose tissue, and plasma triglyceride levels are lowered.
July 16, 2025 at 11:13 PM
Insulin upregulates LIPOPROTEIN LIPASE, which hydrolyzes triglycerides in chylomicrons and VLDL; the liberated fatty acids are largely taken up and esterified in adipose tissue, and plasma triglyceride levels are lowered.
SGLT2 inhibitors (cana,empaglifozin) increase sodium delivery to the macula densa, decreasing renin production and reducing hyperfiltration.
July 16, 2025 at 11:02 PM
SGLT2 inhibitors (cana,empaglifozin) increase sodium delivery to the macula densa, decreasing renin production and reducing hyperfiltration.
Thyroglobulin serves as a source of tyrosine residues for thyroid hormone synthesis.
When thyroid metabolic activity is low, serum thyroglobulin is also low.
When thyroid metabolic activity is low, serum thyroglobulin is also low.
July 16, 2025 at 10:57 PM
Thyroglobulin serves as a source of tyrosine residues for thyroid hormone synthesis.
When thyroid metabolic activity is low, serum thyroglobulin is also low.
When thyroid metabolic activity is low, serum thyroglobulin is also low.
Transitional cell bladder cancer risk factors:
-Cigarette smoking
-Occupational exposure to rubber, plastics, aromatic amine-containing dyes, textiles, or leather.
Squamous cell carcinoma (less common) risk factors
-Schitsosoma haematobium
-Chronic bladder inflammation (catheter)
-Cigarette smoking
-Occupational exposure to rubber, plastics, aromatic amine-containing dyes, textiles, or leather.
Squamous cell carcinoma (less common) risk factors
-Schitsosoma haematobium
-Chronic bladder inflammation (catheter)
July 16, 2025 at 10:53 PM
Transitional cell bladder cancer risk factors:
-Cigarette smoking
-Occupational exposure to rubber, plastics, aromatic amine-containing dyes, textiles, or leather.
Squamous cell carcinoma (less common) risk factors
-Schitsosoma haematobium
-Chronic bladder inflammation (catheter)
-Cigarette smoking
-Occupational exposure to rubber, plastics, aromatic amine-containing dyes, textiles, or leather.
Squamous cell carcinoma (less common) risk factors
-Schitsosoma haematobium
-Chronic bladder inflammation (catheter)
Kyphoscoliosis variant of Ehlers-Danlos syndrome results from an autosomal recessive defect in lysyl hydroxylase, a vitamin C-dependent enzyme involved in the posttranslational modification of procollagen to mature collagen.
July 16, 2025 at 10:48 PM
Kyphoscoliosis variant of Ehlers-Danlos syndrome results from an autosomal recessive defect in lysyl hydroxylase, a vitamin C-dependent enzyme involved in the posttranslational modification of procollagen to mature collagen.
Exercise-induced sympathetic stimulation (sinus tachycardia) on ECG leads to increased frequency of P waves and shortening of the PR interval and R-R interval.
July 16, 2025 at 10:39 PM
Exercise-induced sympathetic stimulation (sinus tachycardia) on ECG leads to increased frequency of P waves and shortening of the PR interval and R-R interval.
Allergen immunotherapy results in desensitization of mast cells, generation of IgG4 neutralizing antibodies, a shift from Th2 to Th1 & regulatory T cells, and decreased levels of IgE production.
July 16, 2025 at 10:32 PM
Allergen immunotherapy results in desensitization of mast cells, generation of IgG4 neutralizing antibodies, a shift from Th2 to Th1 & regulatory T cells, and decreased levels of IgE production.
Adenosine is rapidly metabolized in the blood by erythrocyte and plasma enzymes accounting for its ultrashort half-life (<10 sec).
It is used to abort supraventricular tachycardia by blocking conduction through the AV node.
It is used to abort supraventricular tachycardia by blocking conduction through the AV node.
July 16, 2025 at 10:29 PM
Adenosine is rapidly metabolized in the blood by erythrocyte and plasma enzymes accounting for its ultrashort half-life (<10 sec).
It is used to abort supraventricular tachycardia by blocking conduction through the AV node.
It is used to abort supraventricular tachycardia by blocking conduction through the AV node.