IM PEARLS Flashcards
Underlying cause of Chest Pain in Stable Angina
Fixed atherosclerotic stenosis of coronary arteries - Increased myocardial oxygen demand - LACTIC ACIDOSIS
Precursor lesion of atherosclerosis
FATTY STREAK containing foam cells (macrophages)
Why does pain radiate to the left arm in Stable Angina
Synapses shared with C4 and C5 sensory fibers
What does pain radiating to the upper back (trapezius) indicate?
PERICARDIAL involvement
Major Risk Factors for Chronic Stable Angina
DM, SMOKING, family history of CAD or premature CAD (M<50(F)
Minor Risk Factor for Chronic Stable Angina
Age, Obesity (independent RF), Estrogen Deficiency (Males & Menopaused), Homocysteinemia
Best initial test for Stable Angina; What are the Expected Findings?
ECG showing ST DEPRESSION, FLATTENING OF T WAVES sec to ischemia
Expected Findings on Cardiac Enzymes in Stable Angina
Cardiac Enzymes NOT ELEVATED
Next best step in management of Stable Angina if ECG is nondiagnostic
EXCERCISE STRESS TESTING or Treadmill Stress Test (for MI Risk Stratification: (+) High Risk, (-) Low Risk)
If unable to walk, what stress test will you order in a Stable Angina patient?
DOBUTAMINE or DYPRIDAMOLE Stress Test (Increase Heart Rate and Contractility)
Stable Angina patient has BASELINE ECG ABNORMALITIES, what stress test is appropriate?
NUCLEAR STRESS TEST (Thallium, Sestamibi)
Most Appropriate Treatment in Stable Angina
LIFESTYLE MODIFICATION, OPD: Aspirin, Beta Blockers, Statins, Nitrates - Symptomatic Relief; NO Mortality Risk Reduction
Complications associated with Stable Angina
ACUTE MYOCARDIAL INFARCTION, ANEURYSMS
Patient’s chest pain unrelieved by rest or nitrates
UNSTABLE ANGINA (Crescendo Angina)
If Stress Test is Positive, what is the next Best Step in Management?
ANGIOGRAPHY (Preventive in MI), start ANTICOAGULATION, ASPIRIN, CLOPIDOGREL, NITRATES and BETA BLOCKERS
Underlying pathology in MI
RUPTURED ATHEROSCLEROTIC PLAQUE
Blood vessel involved in Acute MI
LEFT ANTERIOR DESCENDING ARTERY
Heart Wall involved in Acute MI
ANTEROSEPTAL WALL
Heart Wall involved in ECG Leads V1, V2
SEPTAL WALL (supplied by Left Anterior Descending)
Heart Wall involved in ECG Leads V3, V4
ANTERIOR WALL (supplied by Left Anterior Descending)
Heart Wall involved in ECG Leads II, III, aVF
INFERIOR WALL (supplied by Right Coronary Artery)
Heart Wall involved in ECG Leads I & aVL, V5 & V6
LATERAL WALL (supplied by Left Circumflex Artery)
2 Forms of Acute MI: Distinguish the two.
STEMI: Q Waves, new LBBB, ST elevations in 2 or more contiguous leads or chest leads (Noncontiguous Leads=PERICARDITIS); NSTEMI: T Wave inversion, ST Depression
Which patient population will MI present in atypical fashion?
ELDERLY (Autonomic Nervous System manifestations are subtle or irregular) and DIABETICS
Cardiac Enzymes requested in Acute MI
TROPONINS & CM-MB
Rise within 4 hours, detectable for 2 weeks, BEST marker for RECENT MI (artificially increased in CKD)
TROPONINS
Rise within 4 hours, peaks at 24 hours, normalizes in 2-3 days, BEST marker for REINFARCTION
CK-MB
Most Important initial intervention at the ER for Acute MI
MONA - Morphine, Oxygen, Nitrates (CI in Inferior Wall MI due to hypotension sec to decreased preload), Aspirin
GOLD STANDARD in treatment of Acute MI
PERCUTANEOUS CORONARY INTERVENTION (if brought to ER within 90 minutes)
Difference of Management in STEMI & NSTEMI
STEMI: PCI or Thrombolysis if PCI not available (most effective at 6 hours, effective up to 12 hours), anticoagulation with Heparin; NSTEMI: PCI, anticoagulation with Heparin (thrombolysis has NO benefit in NSTEMI)
Absolute Contraindication to Thrombolysis in Acute MI
Hemorrhagic CVD, Brain Tumor, Head Trauma, Ischemic CVD within last 1 year, Active Bleeding (exc Menses), Aortic Dissection, BP Cutoff >180/110mmHg
Medication shown to Improve Acute MI Survival
ASPIRIN, BETA BLOCKERS (Dec Demand), ACE(prevent CHF)/ARBs (if with LV dysfunction)
Acute Complications of Acute MI
PUMP FAILURE (Acute CHF; Inpatients) & ARRHYTHMIAS (Ventricular Fibrillation; Outpatients)
How is Extent of Pump Failure Stratified?
KILLIP CLASSIFICATION - I: No evidence of HF; II: Mild to moderate HF (S3 Gallop, Lung Rales, or JVD); III: Overt pulmonary edema; IV: Cardiogenic Shock
Why is there Pulmonary Edema in Acute MI
PUMP FAILURE (LV Dysfuntion) - Backflow of Blood into Pulmonary Vessels
Associated Complications for Acute MI
Myocardial Aneurysm, Papillary Muscle Rupture, Rupture of Interventricular Septum, Free Wall Rupture, Pericarditis (Dressler Syndrome)
2-7 Days post MI, MCC: Inferior Wall Ischemia, Sx: Pansystolic Murmur radiating to Axilla, Mitral Regurg Murmur, Dx: 2D Echo, Tx: Surgical Repair
PAPILLARY MUSCLE RUPTURE
3-5 days post MI, MCC: Anterior Wall MI, Sx: Acute R-Sided CHF, Harsh holosystolic murmur in LLSB, thrill, Tx: Balloon Catheterization, Surgical Repair
RUPTURE OF IV SEPTUM (Benign)
5 days-2 weeks post MI, MCC: Lateral Wall MI, Sx: Sudden chest pain, Acute HF, Hemopericardium, Tamponade, PEA, Death 90%, Tx: Pericardiocentesis, Emergency Thoracotomy
FREE WALL RUPTURE
1 month post MI, Sx: Persistent ST elevation, Tx: Warfarin, Surgical Repair
MYOCARDIAL ANEURYSM
Weeks to Months post MI, Sx: Pleuritic chest pain, Pericardial Friction Rub, Fever, Tx: High-Dose Aspirin, Ibuprofen (NSAIDS)
DRESSLER SYNDROME
Management for Severe Bleeding upon Heparinization of Acute MI patient
Stop Heparin. Give PROTAMINE SULFATE.
Management of Thrombocytopenia upon Heparinization of Acute MI patient
Stop Heparin. Give LEPIRUDIN/ ARGATROBAN
Underlying cause of Congestive Heart Failure
VENTRICULAR DYSFUNCTION sec to CORONARY ARTERY DISEASE/ HYPERTENSION
Congestive Heart Failure caused by a pulmonary etiology
COR PULMONALE
Histopathologic change of CHF
CONCENTRIC (Inc Cardiac Muscle Width) LV HYPERTROPHY due to Pressure Overload (contrast to Eccentric {Dilation of Chamber} LVH in Hyperthyroidism) & SIDEROPHAGES (Hemosiderin-laden macrophages or HEART FAILURE CELLS)
Forms of CHF
SYSTOLIC (Weak LV) vs DIASTOLIC (hear unable to accommodate, does not relax enough) HF; LOW OUTPUT vs HIGH OUTPUT HF; LEFT-SIDED vs RIGHT-SIDED HF
Differentiaten Systolic from Diastolic Heart Failure
Systolic HF has LOW EF (40-50%)
Differentiate Low from High Output Heart Failure
LOW OUTPUT HF has CO 3L/MIN PER M2 (Hyperthyroidism, Anemia, Beri-Beri, Pregnancy, AV Fistula)
Differentiate Left from Right-Sided HF
Left-Sided HF: PULMONARY CONGESTION, ORTHOPNEA, WEAKNESS; Right-Sided HF: PERIPHERAL EDEMA, CONGESTIVE HEPATOMEGALY, SYSTEMIC VENOUS DISTENTION
Assessment of Functional Status of CHF
NYHA FUNCTIONAL CLASSIFICATION: I- No Limitation of Physical Activity, II- Slight Limitation of Physical Activity, III- Marked Limitation of Physical Activity, IV- Complete Limitation of Physical Activity (Symptomatic even at rest)
Criteria for Diagnosis of CHF
FRINGHAM CRITERIA: MAJOR (PRINCES H) - Paroxysmal nocturnal dyspnea, Rales, Increased CVP, Neck vein distention, Cardiomegaly, acute pulmonary Edema, S3 Gallop, Hepatojugular Reflux; MINOR - bipedal edema, night cough, dyspnea on exertion, hepatomegaly, pleural effusion, decreased vital capacity, tachycardia, weight loss
ORTHOPNEA in CHF
Redistribution of fluid from splanchic circulation and lower extremities into central during recumbency
PAROXYSMAL NOCTURNAL DYSPNEA in CHF
Inc Pressure in Bronchial Arteries -> Airway Compression with Interstitial Pulmonary Edema
Irregular Pattern of Respiration seen in CHF
CHEYNE-STOKE RESPIRATION due to Diminished Sensitivity of Respiratory Center to Arterial PCO2
CRACKLES in CHF
Transudation of fluid from intravascular space into he alveoli
ABDOMINAL PAIN In CHF
Chronic passive congestion of liver lead to distention of Glisson’s Capsule (pain-sensitive)
Most important Diagnostic Test in CHF
2D ECHOCARDIOGRAPHY (EJECTION FRACTION)
Use of Brain Natreuretic Peptide in CHF
Differentiates cardiogenic from noncardiogenic pulmonary edema during shortness of breath (Normal BNP excludes CHF as cause of shortness of breath)
Most likely seen on Chest Xray in CHF
CARDIOMEGALY, PULMONARY CONGESTION (pulmonary vessel markings at apex), KERLEY B LINES
Most important treatment for pulmonary edema in CHF
LOOP DIURETICS (FUROSEMIDE)
Treatment modalities shown to decrease mortality in CHF
ACE-Is/ARBs (EF<35 in FC IV)
Drug that decreases hospitallization but has no effect on overall mortality of CHF patients
DIGOXIN
Heart valve involved in Infective Endocarditis
TRICUSPID VALVE
Most common microbial etiology in Infective Endocarditis
STAPHYLOCOCCUS AUREUS
Complications of Infective Endocarditis
RUPTURE OF CHORDAE TENDINAE, SEPTIC EMBOLISM
Virulence Factor of Causative Organism in IE that conveys Penicillin Resistance
PENICILLINASE
Virulence Factor of the Causative Organism in IE that conveys Complement Inactivation
PROTEIN A
Virulence Factor of Causative Organism in IE that conveys Ability to Cause Chordae Rupture
HYALURONIDASE
Most Common Cause of Acute IE? In IV Drug Abusers?
BOTH STAPHYLOCOCCUS AUREUS
Most Common Cause of Subacute IE? In Native-Valve IE?
BOTH VIRIDANS STREP
Most Common Cause of Prosthetic Valve IE
STAPHYLOCOCCUS EPIDERMIDIS
Most Common Cause of Culture-Negative IE
HACEK
Most Common Cause of IE in Colon Cancer Setting
S. BOVIS (MARANTIC ENDOCARDITIS)
IE in GIT Surgery
ENTEROBIUS FAECALIS
IE in SLE patient setting
LIBMAN-SACKS ENDOCARDITIS or VERRUCOUS ENDOCARDITIS
Best initial test for Infective Endocarditis
TRANSTHORACIC ECHOCARDIOGRAPHY
Other Diagnostic Test may be needed for Diagnosis of IE
BLOOD CULTURES from 2 NON-CONTIGUOUS SITE
Clinical Criteria for Diagnosis of IE
DUKE’S CRITERIA: MAJOR - 2 Positive Blood Culture, Positive Echocardiography (Vegetations); MINOR - Predisposing valve abnormality, Fever, Vascular Phenomena, Immunologic Phenomena, One Positive Culture, Suggestive Echocardiography
Vascular Phenomena associated with IE
MAJOR ARTERIAL EMBOLI, SEPTIC PULMONARY INFARCTS, MYCOTIC ANEURYSM, INTRACRANIAL HEMORRHAGE, CONJUNCTIVAL HEMORRHAGE, SPLINTER HEMORRHAGE, JANEWAY LESIONS
Immunologic Phenomena associated with IE
GLOMERULONEPHRITIS, OSLER’S NODES, ROTH’S SPOTS, RHEUMATOID FACTOR
Most Appropriate Empiric Therapy for IE until Culture is available
VANCOMYCIN + GENTAMICIN
Considered High-Risk Patiets requiring Prophylaxis before a Dental Procedure
PROSTHETIC VALVES, PRIOR IE, UNREPAIRED CYANOTIC CHD, RECENTLY-REPAIRED CHD, INCOMPLETELY-REPAIRED CHD, VALVULOPATHY POST-TRANSPLANT
Drug given for Standard Prophylaxis before Dental Procedures? If patient has Penicillin Allergy?
AMOXICILLIN; if WITH ALLERGY - CLINDAMYCIN or CLARITHROMYCIN
Underlying Cardiac Defect in RHD (Mitral Stenosis)
MITRAL VALVULAR DAMAGE DUE TO PREVIOUS RHEUMATIC FEVER
Histopathologic Changes in the Myocardium in RHD
“2 Russians”: ASCHOFF BODIES (ANITSCHKOW MYOCYTES)
Hemodynamic Changes occuring in the heart in RHD
INCREASED LEFT ATRIAL DIASTOLIC PRESSURE
Acute Rheumatic Fever Diagnosis
JONES CRITERIA: 2 Major or 1 Major & 2 Minor: MAJOR (JONES) - migratory polyarthritis (Joints), pancarditis (Oh my heart!), subcutaneous Nodules, Erythema marginatum, Sydenham’s chorea; MINOR - Arthralgia, Fever, Elevated ESR/CRP, Prolonged PR interval
Infection usually preceding ARF
STREPTOCOCCUS PYOGENES (GABHS) INFECTIONS - SKIN (IMPETIGO) or PHARYNGITIS
Pathophysiologic Mechanism of ARF
TYPE II REACTION ( IMMUNOLOGIC CROSS-REACTION due to STREPTOCOCCAL M PROTEIN)
Long term sequelae of repeated bouts of ARF characterized by Permanent Valvular Damage
RHEUMATIC HEART DISEASE
Most common Valvular Defects in ARF
MITRAL REGURGITATION
Most Common Valvular Defects in RHD
MITRAL STENOSIS
Best initial Test for RHD
2D ECHOCARDIOGRAPHY
Most Appropriate Treatment for RHD
SURGICAL REPAIR (VALVOTOMY, COMMISUROTOMY), ANTICOAGULATION, DIURETICS
Most common Valvular Heart Disease
MITRAL VALVE PROLAPSE (Most Common), MITRAL STENOSIS, MITRAL REGURGITATION, AORTIC STENOSIS, ATRIAL REGURGITATION
Conditions associated with MVP
EHLERS-DANLOS SYNDROME, MARFA. SYNDROME, POLYCYSTIC KIDNEY DISEASE
Murmur of MVP
MIDSYSTOLIC CLICK followed by MIDSYSTOLIC to LATE SYSTOLIC MURMUR at APEX
Murmur of Mitral Stenosis
OPENING SNAP followed by MID-DIASTOLIC RUMBLE, LOUD S1 and P2
Clinical Presentation of Mitral Stenosis
Usually ASYMPTOMATIC until ATRIAL FIBRILLATION or PREGNANCY develops
Murmur of Mitral Regurgitation
HOLOSYSTOLIC MURMUR at APEX radiating to AXILLA
Other signs of Mitral Regurgitation
HYPERDYNAMIC PRECORDIUM, BRISK CAROTID UPSTROKE
Murmur of Aortic Stenosis
EARLY SYSTOLIC EJECTION MURMUR at 2ND RIGHT ICS, radiating to CAROTIDS
Signs of Severe Aortic Stenosis
GALLAVARDIN PHENOMENON (Murmur disappears over sternum, reappears in apex) & PULSUS PARVUS ET TARDUS (small or weak pulse that rises slowly and delayed in occurence)
Murmur of Aortic Regurgitation
CORRIGAN PULSE: rapid rise and fall of carotid pulse; QUINCKE PULSE: subungual cappilary pulsations; DUROZIEZ SIGN: diastolic murmur over partially-compressed femoral artery; DE MUSSET SIGN: headbobbing with heartbeat; HILL SIGN: systolic BP >30mmHg in legs than arms; TRAUBE SIGN: pistol shot femoral pulses
Effect of Valsalva On murmur
INCREASES INTRATHORACIC PRESSURE, DECREASING VENOUS RETURN, DECREASING THE INTENSITY OF MURMURS
Effect of Squatting on Murmur
INCREASES VENOUS RETURN, INCREASING INTENSITY OF MURMURS
Pathophysiologic Type of Pericarditis
SEROUS, FIBRINOUS & HEMORRHAGIC
Most common infectious etiology of Pericarditis
COXSACKIE VIRUS TYPE B
Best initial test for Pericarditis? What are Expected Findings?
ECG showing DIFFUSE ST ELEVATIONS and PR DEPRESSION
Most appropriate treatment for Pericarditis
NSAIDS
Triad of Cardiac Tamponade
BECKS TRIAD: HYPOTENSION, JVD, DISTANT/MUFFLED HEART SOUNDS
Other Classic Signs of Cardiac Tamponade
PULSUS PARADOXUS (>10 mmHg fall in BP with inspiration), KUSSMAUL SIGN (sharp increase in JVP with inspiration), EWART SIGN (dullness, increased fremeti, egophony at left scapula), WATER BOTTLE HEART
ECG findings in Cardiac Tamponade
DECREASED QRS VOLTAGE AND ELECTRICAL ALTERNANS
Most appropriate treatment for Cardiac Tamponade
PERICARDIOCENTESIS
Differentiate Constrictive from Acute Pericarditis
CONSTRICTIVE PERICARDITIS PRESENTS WITH JVD, SIGNS OF RIGHT-SIDED HF and PERICARDIAL KNOCK (CALCIFIED OR CASTED PERICARDIUM)
Best initial step for Constrictive Pericarditis? Expected finding?
TRANSTHORACIC ECHOCARDIOGRAPHY showing INCREASED PERICARDIAL THICKNESS with CALCIFICATION
Most appropriate treatment for Constrictive Pericarditis
MILD CASES: Diuretics, ACE-Inhibitors SEVERE CASES: Pericardiectomy
Underlying cause for Acromegaly
Pituitary tumor secreting excess amount of GH
Important thing to compare in Acromegaly
COMPARE CURRENT APPEARANCE WITH OLD PHOTOS TO SEE DIFFERENCE IN FACI FEATURES
Loss of Peripheral Vision in Acromegaly
PITUITARY TUMOR compressing the OPTIC CHIASM, causing BITEMPORAL HEMIANOPSIA
Prone to Develop Carpal Tunnel Syndrome in Acromegaly
BONE OVERGROWTH COMPRESSES MEDIAN NERVE
Best initial test for Acromegaly
SERUM IGF-1 LEVELS
Best confirmatory Test for Acromegaly
SERUM GH after an OGTT (Glucose normally suppresses GH)
Most appropriate management for Acromegaly
TRANSSPHENOIDAL RESECTION OF TUMOR
Drug may be Given preoperatively to Shrink tumor size in Acromegaly
OCTREOTIDE (SOMATOSTATIN ANALOGUE)
Underlying cause for Prolactinoma
Pituitary tumor secreting excess amounts of PROLACTIN (antagonistic of GnRH)
Amenorrhea in Prolactinoma
DECREASED GnRH -> DEC FSH & LH -> INTERRUPTION OF MENSTRUAL CYCLE
Physiologic downregulators of Prolactin Secretion
DOPAMINE (antagonistic of Prolactin), ESTROGEN, PROGESTERONE, SOMATOSTATIN
Best initial management for Prolactinoma
Drug therapy with BROMOCRIPTINE or CABERGOLINE (DOPAMINE AGONISTS)
Drugs known to cause Secondary HyperProlactinemia
METOCLOPRAMIDE, AMITRYPTILINE, PHENOTHIAZINES, ANTIPSYCHOTICS
Underlying cause of SIADH
LUNG CANCER COMPOSED OF NEUROENDOCRINE CELLS -> AUTONOMOUS PRODUCTION OF EXCESS ADH
Decreased Sodium in SIADH
INCREASED WATER RETENTION -> DILUTIONAL HYPONATREMIA
Seizures in SIADH
Decreased Sodium creates osmotic gradient causing water movement into the brain -> CEREBRAL EDEMA
Underlying cause of DI
HEAD TRAUMA caused DESTRUCTION of the POSTERIOR PITUITARY GLAND
2 Types of DI
CENTRAL DI due to ADH Deficiency and NEPHROGENIC DI due to UNRESPONSIVENESS TO ADH
Distinguish between Central DI & Nephrogenic DI
WATER DEPRIVATION TEST: CENTRAL DI - Increased Urine Osmolality after ADH administration at the 6th hour of test; NEPHROGENIC DI - No increase in Urine Osmolality after ADH Administration at the 6th hour of test; PSYCHOGENIC POLYDIPSIA - increasing Urine Osmolality even if before ADH admin and further increase after ADH admin
Treatment for DI
CENTRAL DI: Give VASOPRESSIN; NEPHROGENIC DI: administer THIAZIDES (dec urine flow to DCT -> induce formation of functional ADH)
Drugs notorious for causing Nephrogenic DI
LITHIUM, DEMECLOCYCLINE
Underling cause for Grave’s Disease
AUTOANTIBODIES STIMULATE HYPERSECRETION OF THYROID HORMONES
Autoantibodies present in Grave’s
ANTI-TSH RECEPTOR ANTIBODIES
Drugs that cause similar condition as Grave’s
AMIODARONE, CLOFIBRATE, METHADONE
Drug of Choice for Grave’s? Feared Side Effect?
THIONAMIDES (PTU, MM); SE - AGRANULOCYTOSIS
Most Appropriate Diagnostic Test for Grave’s? Expected results?
Free T4, TSH (Increased FT4, Decreased TSH)
Most Appropriate Treatment for Grave’s
RADIOACTIVR IODINE ABLATION THERAPY
Expected treatment Complication of RAI used in Grave’s
SECONDARY HYPOTHYROIDISM
Drugs given preoperatively if Surgical Intervention contemplated in Grave’s
IODIDES to decrease Gland Vascularity
TRH Decrease, TSH Decrease, T4 Increase (Target Organs)
PRIMARY HYPERTHYROIDISM
TRH Decreased, TSH Increased, T4 Increased (Pituitary Problem)
SECONDARY HYPERTHYROIDISM
TRH Increased, TSH Increased, T4 Increased (Hypothalamic Problem)
TERTIARY HYPERTHYROIDISM
Weight Loss in Grave’s
EXCESS T3/T4 -> Increased CATABOLISM
Increased Sweating, Increased Bowel Movement & Tachycardia in Grave’s
EXCESS T3/T4 -> SYMPATHETIC OVERACTIVITY
Irregular Menses in Grave’s
EXCESS T3/T4 -> Inc Sex Hormone Binding Globulin levels, Inc Total Serum Estrogen -> Inc LH and Decreasing mid-cycle LH surge
Exophthalmos in Grave’s
Increased Volume of Retrobulbar Tissue due to Deposition of GAGs as a result of Lymphoytic Infiltration
Fine Finger Tremors in Grave’s
EXCESS T3/T4 -> Inc Synaptic Transmission and Inc Cerebration -> Reflex Oscillation of Muscle Spindles
Underlying Cause of Hypothyroiditis
Antibodies against Thyroglobulin and Thyroid Peroxidase lead to Autoimmune Destruction of Thyroid Gland
TRH Increased, TSH Increased, T4 Decreased (Target Organ Problem)
PRIMARY HYPOTHYROIDISM
TRH Increased, TSH Decreased, T4 Decreased (Pituitary Problem)
SECONDARY HYPOTHYROIDISM
TRH Decreased, TSH Decreased, T4 Decreased (Hypothalamic Problem)
TERTIARY HYPOTHYROIDISM
Fatigue and Weight Gain in Hypothyroidism
LOW T3/T4 -> DECREASED METABOLISM
Bradycardia in Hypothyroidism
LOW T3/T4 -> DECREASED SYMPATHETIC DRIVE
Coarse, Dry Skin in Hypothyroidism
LOW T3/T4 -> DECREASED HEAT PRODUCTION and DECREASED SWEATING
Depression in Hypothyroidism
LOW T3/T4 -> DECREASED SYNAPTIC TRANSMISSION IN BRAIN and DECREASED PRODUCTION OF NEUROTRANSMITTERS (SEROTONIN)
Amenorrhea in Hypothyroidism
LOW T3/T4 -> INCREASED TRH -> INC PROLACTIN, DEC GnRH, DEC FSH/LH
Bilateral Eyelid Edema
DEPOSITION OF GAGS as a result of LYMPHOCYTIC INFILTRATION of the CONNCECTIVE TISSUE of the SKIN
Underlying Cause of Hyperparathyroidism
PARATHYROID TUMOR SECRETING LARGE AMOUNTS OF PTH into BLOODSTREAM
Increased PTH, Increased s. Calcium, Decreased s. Phosphate (Target Organs Problem)
PRIMARY HYPERPARATHYROIDISM
Increased PTH, Decreased s. Calcium, Decreased s. Phosphate
SECONDARY HYPERPARATHYROIDISM (Pituitary Problem)
Depression and Fatigue in Hyperparathyroidism
UNKNOWN
Kidney Stones in Hyperparathyroidism
INCREASED URINARY CALCIUM CONCENTRATION
Muscle Weakness in Hyperparathyroidism
EXCESS PTH -> INCREASED PROTEIN BREAKDOWN and MUSCULAR ATROPHY
Other Expected Symptoms in Hyperparathyroidism
PAINFUL BONES, RENAL STONES, ABDOMINAL GROANS, PSYCHIATRIC OVERTONES
Most Appropriate Treatment in Hyperparathyroidism
SURGICAL PARATHYROIDECTOMY
Structure Injured during Surgical Treatment of Hyperparathyroidism
RECURRENT LARYNGEAL NERVE
Malignancy may Present Similarly with Hyperparathyroidism
HYPERCALCEMIA OF MALIGNANCY (usually SCCA OF LUNGS) due to PRODUCTION OF PTHrp (related protein)
Other Diseases that can Result in Secondary Forms of Hyperparathyroidism
CHRONIC KIDNEY DISEASE, CHRONIC PANCREATITIS. MALABSORPTION
Underlying Cause of Hypoparathyroidisn
INADVERTENT REMOVAL OF THE PARATHYROID GLAND DURING THYROID SURGERY
Decreased PTH, Decreased s. Calcium, Increased s. Phosphate
PRIMARY HYPOPARATHYROIDISIM
Decreased PTH, Increased s. Calcium, Increased s. Phosphate
SECONDARY HYPERPARATHYROIDISM
Muscle Twitching in Hypoparathyroidism
LOW SERUM CALCIUM -> INCREASED EXCITABILITY OF MOTOR NEURONS by DECREASING THRESHOLD POTENTIAL (HYPOCALCEMIC TETANY)
Underlying Cause of DM I
AUTOIMMUNE DESTRUCTION OF BETA CELLS IN PANCREAS, LEADING TO INSULIN DEFICIENCY
Increased Glucose, Decreased Insulin, Decreased C Peptide
TYPE 1 DM