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275 Cards in this Set

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What is the antidote:

Acetaminophen
N-acetylcysteine
What is the antidote:

Anticholinergics
Physostigmine
What is the antidote:

Benzodiazepines
Flumazenil
What is the antidote:

Beta Blockers
Glucagon and calcium
What is the antidote:

Carbon Monoxide
Oxygen
What is the antidote:

Cyanide
Amyl nitrate
What is the antidote:

Digoxin
Anti-digoxin Fab antibodies
What is the antidote:

Ethylene Glycol
Ethanol
What is the antidote:

Heparin
Protamine
What is the antidote:

Iron
Deferoxamine
What is the antidote:

Isoniazid
Pyridoxine
What is the antidote:

Lead
EDTA or BAL
What is the antidote:

Methanol
Ethanol
What is the antidote:

Opioids
Naloxone
What is the antidote:

Warfarin
Vitamin K
What is the antidote:

Organophosphates
Atropine or Pralidoxime (2-PAM)
What are the symptoms of anticholinergic overdose?
Anhidrosis
Fever
Delirium
Mydriasis

"Dry as a bone, Mad as a hatter, Blind as a bat, Hot as a hare"
What are the symptoms of opiate overdose?
Miosis
Out of it (sedation)
Respiratory depression
Pneumonia (aspiration)
Hypotension
Infrequency (constipation, urinary retention)
Nausea
Emesis

MORPHINE
What is benzodiazepine used for?
Sedative/Tranquilizer
Antidote to alcohol withdrawal
What does an overdose of acetominophen do?
Liver failure
What does an overdose of benzodiazepines cause?
Sedation
Respiratory depression (life threatening)
What does methanol ingestion cause?
Severe abdominal pain
Blindness (can be permanent)

Found in antifreeze, "wood alcohol," improperly fermented alcohol
What does ethylene glycol ingestion cause?
Renal failure
What is the cause of death in carbon monoxide poisioning?
Directly inhibits electron transport chain (respiration) in mitochondria by binding to hemoglobin with greater affinity than oxygen
What is the effect of cyanide ingestion?
Symptoms:
Drowsiness
Tachycardia
Coma

Reacts with and inactivates respiratory enzymes, preventing production of ATP
What are the symptoms of cholinergic overdose? (organophosphates)
Salivation
Lacrimation
Urination
Defecation
GI upset
Emesis

SLUDGE
Mechanism of Action:

Penicillins and Cephalosporins
Inhibit peptide cell wall synthesis
Mechanism of Action:

Aminoglycosides
Inhibit initiation of translation

Only kill aerobic gram neg bacteria

Ototoxic - risk increased with use of loop diuretics
List some aminoglycosides
Gentamicin
Amikacin
Neomycin
Streptomycin
Tobramycin
Mechanism of Action:

Vancomycin (glycopeptide antibiotic)
Inhibits phospholipid plasma membrane synthesis and peptidoglycan polymerization

Inhibits cell membrane and cell wall synthesis
Mechanism of Action:

Quinolones
Inhibit Topoisomerase

Inhibit bacterial ability to use its own DNA
What are the adverse effects of quinolones?
Contraindicated under age 16 (effects on cartilage in joints)

Use with caution over age 60 (increased risk of tendinopathy, rupture)

Prolong QT interval
Mechanism of Action:

Chloramphenicol
Inhibits peptidyl transferase

Inhibits protein synthesis
Mechanism of Action:

Macrolides (Erythromycin class)
Inhibit protein synthesis
Mechanism of Action:

Tetracyclines
Inhibit tRNA binding

Inhibit protein synthesis
Name some tetracyclines
Doxycycline
Tetracycline
Minocycline
Tigecycline
Mechanism of Action:

Sulfonamides
Inhibit folate synthesis
Mechanism of Action:

Trimethoprim
Inhibits folate use
Mechanism of Action:

Bacitracin
Inhibits cell wall synthesis
How is bacitracin used?
Only topical

Very nephrotoxic
What is polymyxin used for?
Antipseudomonal

Only topical, usually ophthalmic
Mechanism of Action:

Carbapenems
Inhibit cell wall synthesis (very powerful)

Effective against most gram pos and many gram neg, aerobic and anaerobic
Name some carbapenems
Doripenem
Ertapenem
Imipenem
Meropenem
Mechanism of Action:

Glycopeptides
Inhibit cell wall synthesis

Teicoplanin and Vancomycin

Only gram pos, usually reserved for serious infections
Mechanism of Action:

Clindamycin
Inhibits protein synthesis
Mechanism of Action:

Metronidazole
Activates mechanisms that destroy microbial DNA

Anaerobic bacteria and protozoa
Mechanism of Action:

Nitrofurantoin (nitrofuran)
Inhibits bacterial enzyme systems

Accumulates in urine - used for UTI
What are the most common bleeding disorders?
Inherited: VonWillebrand's

Acquired: Vitamin K deficiency
Von Willebrand Disease
Lack of factor VIII-R

Features:
aPTT prolonged
Bleeding time prolonged
Hemophilia A
Lack of factor VIII

Features:
aPTT prolonged
Normal bleeding time
Hemophilia B
Lack of factor IX

Features:
aPTT prolonged
Normal bleeding time
Vitamin K deficiency
Affects factors II, V, VII, IX, X

Features:
PT prolonged
Fat malabsorption
Idiopathic Thrombocytic Purpura (ITP)
Features:
Immune mediated
Usu. follows viral infection in children, can be chronic in adults
Thromotic Thrombocytic Purpura (TTP)
Features:
Usu. young women
Microthrombi
Fragmented RBCs (helmet cells)
What does bleeding time test?
platelet function
What does PT test?
Extrinsic and Common pathways
What does aPTT test?
Intrinsic and Common pathways
What does TT test?
Common pathway only
Spherocytosis
Autosomal Dominant hemolytic anemia

Features:
Defective spectrin
Splenomegaly
G6PD Deficiency
Hemolytic anemia caused by hemolysis due to oxidative stress (reaction to viral infection, fava beans, sulfa drugs, quinine, nitrofurantoin)

Features:
Heinz bodies (hemoglobin degradation products)
Sickle Cell Anemia
HbS (2 alpha, 2 beta S)

Sickling triggered by: hypoxia, dehydration, acidosis

Can cause vaso-occlusive crisis, aplastic crisis, sequestration crisis (splenomegaly), autosplenectomy
alpha-Thalassemias
HbH (4 beta)

Common in Southeast Asia

Features:
Hypochromic cells
Target cells
beta-Thalassemias
HbA2 (2 alpha, 2 delta) and HbF (2 alpha, 2 gamma)

Common in Mediterranean and US

Features:
Hypochromic cells
Target cells

Homozygous = major, heterozygous = minor
Immune Mediated Hemolytic Anemia with Warm Antibodies
Usually IgG

Active at 37 degrees C

Drugs
Malignancies
SLE
Immune Mediated Hemolytic Anemia with Cold Antibodies
Usually IgM

Most active at 0-4 degrees C

Mycoplasma pneumonia
Mononucleosis
Lymphoma

Agglutination occurs in peripheral (cool) parts of body - causes vascular obstruction (Raynaud's phenomenon)
What is the Coombs test?
Direct: Mix patient's RBCs with anti-IgG
Detects cell bound antibodies

Indirect: Mix patient's plasma with normal RBCs
Detects free antibodies
Megaloblastic Anemia
Features:
Hypochromic, macrocytic RBCs
Hypersegmented neutrophils

Caused by Folate deficiency: anemia only
Caused by B12 deficiency: anemia PLUS neurological symptoms
Iron Deficiency Anemia
Usu. from chronic blood loss (in elderly pts, suspect colorectal malignancy)

Features:
Hypochromic, microcytic RBCs
Aplastic Anemia
Caused by bone marrow failure due to viral infections, toxins, drugs (alkylating agents, chloramphenicol)
Plummer-Vinson Syndrome
Anemia
Atrophic glossitis
Esophageal webs (cause dysphagia)
Fanconi Anemia
Autosomal Recessive

Hypoplastic thumbs
Absent radii
Aplastic anemia

Bone marrow DNA more susceptible to radiation and alkylating agents
Special Feature of RBC:

Heinz Bodies
Denatured hemoglobin

G6PD deficiency
Special Feature of RBC:

Howell-Jolly Bodies
Nuclear fragments

Post-splenectomy
Special Feature of RBC:

Basophil Stippling
Small dots on periphery of RBC - accumulations of rRNA

Lead poisoning
Special Feature of RBC:

Siderocytes (Pappenheimer Bodies)
Dense purple-blue granules within RBC

Iron overload
Special Feature of RBC:

Reticulocytes
Remains of ribosomal RNA

Increased production/release of RBCs
Recovery from hemorrhage
What is the reticulocyte index?
Relate reticulocyte count to hematocrit to correct for blood loss

Important following acute blood loss - reticulocyte count can double in first 24hrs, so important to correct
Which drugs cause most drug induced neutropenia?
Alkylating agents
Chloramphenicol
Chlorpromazine
Sulfonamides
Phenylbutazone
Leukocytosis:

Neutrophils
Acute infections
Stress
Leukocytosis:

Eosinophils
Allergy
Asthma
Parasitic infections
Leukocytosis:

Lymphocytes
Tuberculosis
Viral infections
Leukocytosis:

Monocytes
Tuberculosis
Malaria
Rickettsia
Acute Lymphoblastic Leukemia (ALL)
Children

Fever
Petechiae
Ecchymoses
CNS infiltrate

Lymphoblasts

Prognosis: Good
Acute Myeloid Leukemia (AML)
Any age

Fever
Petechiae
Ecchymoses
Lymphadenopathy
Splenomegaly

Auer rods in myeloblasts

Prognosis: depends on type
Chronic Myelogenous Leukemia (CML)
Young adults

Fever
Night sweats
Splenomegaly *

Philadelphia chromosome

Prognosis: Poor
Chronic Lymphocytic Leukemia (CLL)
Elderly

Insidious
Few symptoms
Low Ig levels
Infections

Lymphocytes predominate

Prognosis: Fair
Hairy Cell Leukemia
Hepatomegaly
Splenomegaly

Pancytopenia
TRAP stain

Prognosis: Poor
What is the Philadelphia chromosome?
c-abl proto-oncogene on chromosome 9 when translocated to the bcr region of chromosome 22 to form a fusion gene bcr/abl

Encodes protein with high tyrosine kinase activity

If present, better prognosis for CML
What is Trousseau's Sign?
Migratory venous thrombosis

Associated with neoplasms
What are the key features of atherosclerosis?
In large to medium arteries
Fatty streaks
Atheromas
What are the key features of Monckeberg's Arteriosclerosis?
Calcific stenosis of the media
"Gooseneck" lumps
In small to medium arteries
Asymptomatic
What are the key features of hyperplastic arteriosclerosis?
Fibrinoid necrosis
Malignant hypertension
"Onion skin" hyperplasia
What are the key features of hyaline arteriosclerosis?
Diabetes mellitus
Thickened basement membrane
Describe the pathogenesis of arteriosclerosis.
Vascular epithelium is injured

Lipids and platelets adhere to injured surface

Leukocytes and platelets release growth factors, triggering smooth muscle proliferation

Macrophages become foam cells

Foam cells aggregate to form fatty streaks, the beginning formation of an atherosclerotic plaque
What are the key features of hypersensitivity arteritis?
In small vessels
Lesions all at same stage
Cryoglobulins
Associated with Henoch-Schonlein Purpura
What are the key features of polyarteritis nodosa?
In small to medium vessels
Kidneys, heart, muscles, skin
Can be fatal but responds well to steroid treatment
What are the key features of thromboangiitis obliterans (Buerger's)?
In small to medium vessels
Smokers
What are the key features of giant cell arteritis?
Temporal Artery:
Sudden blindness
Female > Male
Associated with polymyalgia rheumatica
What are the key features of Wegener's?
Upper respiratory vasculitis
Lower respiratory vasculitis
Glomerulonephritis
What are the key features of Takayasu?
"Pulseless Disease"
In aorta or large arteries
Asian females
What are the key features of Kawasaki?
Mucouctaneous lymph node syndrome
Coronary artery aneurysms
Fever, conjunctivitis, maculopapular rash
Japanese children
What are the key features of atherosclerotic aneurysms?
Fusiform
In abdominal aorta
Hypertension
What are the key features of syphilitic aneurysms?
Saccular
In ascending aorta
Associated with aortic insufficiency
What are the key features of dissecting aneurysms?
In aorta (ascending or descending)
Hypertension
Marfan syndrome

Not a true aneurysm
What are the key features of berry aneurysms?
Congenital
In circle of Willis
Associated with polycystic kidney disease (adult form)
What are the key features of micro aneurysms?
Cerebral - Hypertension
Retinal - Diabetes
Heart Sounds:

Mitral Valve Prolaps
Midsystolic click

Occurs in young women, Marfan syndrome
Heart Sounds:

Mitral Stenosis
Diastolic rumble

Occurs in rheumatic heart disease, atrial fibrillation
Heart Sounds:

Mitral Regurgitation
Holosystolic murmur
Transmitted to axilla

Occurs in MI of papillary muscle, acute rheumatic fever, endocarditis
Heart Sounds:

Aortic Stenosis
Systolic murmur
Transmitted to carotid arteries
Pulsus tardus

Can be congenital or caused by degenerative calcifications
Heart Sounds:

Aortic Regurgitation
Diastolic murmur
"Pistol shots" in femoral artery
"Water hammer" pulse
Heart Sounds:

Patent Ductus Arteriosus
Continuous murmur
"Machine like"
What are the acyanotic heart defects?
Left to Right

VSD (most common)
ASD
PDA
What are the cyanotic heart defects?
Right to Left

Tetralogy of Fallot (most common)
Transposition of the great vessels
Persistent truncus arteriosus
Eisenmenger (reversal of L to R shunt due to pulmonary hypertension)
What are the obstructive heart defects?
Coarctation of the aorta (preductal in infants, postductal in adults)
Pulmonary stenosis or atresia
Aortic stenosis or atresia
What is TORCH?
Toxoplasmosis
Rubella
CMV
Herpes
Common Congenital Defects:

Fetal Alcohol Syndrome
Cardiac defect
Microcephaly
Short upturned nose with long philtrum
Common Congenital Defects:

Fetal Hydantoin Syndrome
Cardiac defect
Microcephaly
Nail hypoplasia
Common Congenital Defects:

Isotretinoin (vitamin A)
Cardiac defect
Hydrocephalus
Cleft palate
Common Congenital Defects:

TORCH (intrauterine infection)
Cardiac defect
Microcephaly
Auditory and visual defects
Common Congenital Defects:

Syphilis
Cardiac defect
Bullous skin lesions (palms, soles)
Hutchinson's teeth (serrated-looking edges)
Saber shins
What is the Tetralogy of Fallot?
Pulmonary artery stenosis
Overriding aorta
VSD
Right ventricular hypertrophy
Signs and Treatment:

Stable Angina
Triggered by exercise/exertion
ST depression
Relieved by rest

TX: Nitroglycerin
Signs and Treatment:

Unstable Angina
Occurs at rest
Crescendo like
Often leads to MI

Unresponsive to nitroglycerin
Signs and Treatment:

Prinzmetal's Angina
Occurs at rest
ST elevation

TX: Calcium antagonists
Signs and Treatment:

Myocardial Infarction
Occurs during exercise/exertion or REM sleep
ST elevation
T inversion

TX: Nitroglycerin, morphine, lidocaine
Gross and Microscopic Changes After MI:

30 min
Gross: none

Micro: mitochondrial swelling
Gross and Microscopic Changes After MI:

4-12 hours
Gross: none

Micro: edema
hemorrhage
Gross and Microscopic Changes After MI:

18-24 hours
Gross: pallor

Micro: neutrophilic infiltrate
Gross and Microscopic Changes After MI:

24-72 hours
Gross: pallor

Micro: coagulation necrosis
loss of nuclei
heavy neutrophil infiltrate
Gross and Microscopic Changes After MI:

3-7 days
Gross: central softening
hyperemic borders

Micro: resorption of dead myofibers
Gross and Microscopic Changes After MI:

10 days
Gross: soft and yellow hyperemic borders

Micro: granulation tissue
Gross and Microscopic Changes After MI:

8 weeks
Gross: gray and firm scar

Micro: scar
What is the most common causes of death in the first hours after an MI?
Arrhythmia (most common)
Congestive heart failure
Cardiogenic shock
Muscle rupture (least common, highest risk 1-2 weeks after MI)
What are the causes of left sided heart failure? The consequences?
Causes:
Ischemic heart disease
Arterial hypertension
Valvular disease

Consequences:
Pulmonary congestion (dyspnea, orthopnea)
Renal hypertension (salt retention)
What are the causes of right sided heart failure? The consequences?
Causes:
Left sided heart failure
Lung disease
Primary pulmonary hypertension

Consequences:
Increased venous pressure leads to:
Edema
Liver congestion
Ascites
Key Features Of:

Acute Endocarditis (Infective)
Caused by Staph aureus, Strep
Previously normal valves
Janeway lesions (non-tender macular patches on palms and soles - septic emboli)
High fever, chills, hematuria
Key Features Of:

Subacute Endocarditis (Infective)
Caused by Strep viridans, gram neg bacilli
Previously abnormal valves
Roth spots (oval retinal hemorrhages with pale center)
Osler nodes (red tender lesions on finger and toe pulps)
Low grade fever
Key Features Of:

Marantic Endocarditis (Noninfective)
Associated with chronic illnesses
Thrombotic
Key Features Of:

Libman Sacks Endocarditis (Noninfective)
Associated with SLE
Verrucous lesions on both sides of valve leaflets
Key Features Of:

Fibrinous Pericarditis
Transmural myocardial infarction
Dressler Syndrome (delayed pericarditis 2-10 wks after MI, due to autoantibodies - responds well to corticosteroids)
"Bread and butter" appearance
Key Features Of:

Serous Pericarditis
Viral infections (often Coxsackie)
Uremia
Key Features Of:

Suppurative Pericarditis
Bacterial infections
Fungal infections
Parasitic infections
What are the clinical signs of pericarditis?
Low grade fever
Pericardial friction rub
Chest pain aggravated by movement of trunk
Pulsus paradoxus (inspiratory fall of BP that is exaggerated)
Who does rheumatic fever occur in?
School-age children with untreated Strep pharyngitis
Key Features Of:

Acute Rheumatic Fever
1-4 wks after tonsillitis
Group A beta-hemolytic streptococci
Children 5-15 yrs
Key Features Of:

Rheumatic Heart Disease
Occurs many years after rheumatic fever
Often asymptomatic
Fibrotic, deformed calcified lines of closure on valve leaflets
Mitral valve > Aortic valve
What are the carditis of rheumatic fever?
Pericarditis (serous effusions)
Myocarditis (heart failure)
Endocarditis (valve damage)
What is an Aschoff Body?
Granuloma
Focal interstitial myocardial inflammation
Found with enlarged macrophages (Anitschkow cells)
What are the Major Jones Criteria?
For diagnosing rheumatic fever

Polyarthritis
Erythema
Subcutaneous nodules
Chorea
Carditis
Key Features Of:

Emphysema
Obstructive lung disease
"Pink puffers"
Barrel chest

Panacinar
Centrilobular

Associated with:
Alpha-1 antitrypsin deficiency in lower lobes
Smoking in upper lobes
Key Features Of:

Chronic Bronchitis
Obstructive lung disease
"Blue bloaters"

Chronic irritation or infection
Hypertrophy of submucosal glands
Key Features Of:

Asthma
Obstructive lung disease
Expiratory wheezing

Types:
Extrinsic - triggered by allergens
Intrinsic - triggered by cold and exercise
Aspirin induced
Key Features Of:

Bronchiectasis
Obstructive lung disease
Result of chronic infections
Kartagener's - immotile cilia
What characterizes obstructive lung disease?
Reduced airflow due to high resistance or low elastic recoil

FRC and TLC are high
What is the REID Index?
Ratio between thickness of submucosal mucus secreting glands and wall thickness between epithelium and cartilage

Used for research and autopsy only (not for diagnosis)
Key Features Of:

Adult ARDS
Restrictive lung disease
Acute diffuse alveolar damage

Caused by:
Shock
Sepsis
Pancreatitis
Toxins
Key Features Of:

Neonatal ARDS
Restrictive lung disease
Insufficient lecithin synthesis by type 2 pneumocytes
Key Features Of:

Pneumoconiosis
Restrictive lung disease

Caused by:
Coal - "tattooing," black sputum
Anthracosis - carbon dust
Asbestosis - fibrous silicates, dry cough
Berylliosis - type IV hypersensitivity
What characterizes restrictive lung disease?
High elastic recoil of lungs

FRC, VC, TLC are low
Key Features Of:

Hypersensitivity Pneumonitis
Restrictive lung disease

Acute - type III - fever, cough, dyspnea, leukocytosis
Chronic - type IV - peribronchial granulomas
Farmer's lung, pigeon breeder's lung, etc
Key Features Of:

Goodpasture Syndrome
Restrictive lung disease

Type II hypersensitivity - antibodies against basal membrane
Hemoptysis, rapidly progressive glomerulonephritis
Key Features Of:

Pulmonary Hemosiderosis
Restrictive lung disease

Type II hypersensitivity - antibodies against basal membrane
Hemoptysis, no renal involvement
Key Features Of:

Alveolar Proteinosis
Restrictive lung disease

Overproduction of surfactant like material
Key Features Of:

Eosinophilic Pneumonia
Restrictive lung disease

Acute (Loffler's) - Type I hypersensitivity
Chronic
Key Features Of:

Diffuse Idiopathic Fibrosis
Restrictive lung disease
Interstitial pneumonitis and fibrosis
Hyperplasia of type II pneumocytes
Key Features Of:

Collagen Vascular Disorders
Restrictive lung disease

Scleroderma
SLE
Wegener's
RA
etc
Where is the alar ligament?
Connects sides of odontoid process (on C2) to lateral aspects of foramen magnum
Where is the transverse ligament (cervical spine)?
Between C1 lateral masses - holds dens in place
Located posterior to dens
What are the components of the cervical cruciform ligament?
Transverse ligament - across dens
Superior band - from transverse ligament to occiput
Inferior band - from transverse ligament to body of C2
What is the tectorial membrane?
Superior continuation of posterior longitudinal ligament
Lies posterior to cruciform ligament
Passes from C1 to internal surface of occipital bone
Where are the anterior and posterior longitudinal ligaments?
Anterior - runs over anterior of spine
Posterior - runs over posterior of vertebral bodies, anterior to spinal cord
What is the function of the scalene muscles?
Unilateral contraction - sidebend neck
Bilateral contraction - flex neck
Anterior and middle - elevation of first rib in forced respiration
Posterior - elevation of second rib in forced respiration
What is the motion of the OA joint?
"Yes" joint
Flexion - Extension

Rotation and sidebending opposite
What is the motion of the AA joint?
"No" joint
Rotation

Rotation and sidebending opposite
What is the motion of the upper cervical spine?
Primarily rotation

Rotation and sidebending same
What is the motion of the lower cervical spine?
Primarily sidebending

Rotation and sidebending same
Autoantibody:

Autoimmune Hemolytic Anemia
Anti-RBC
Autoantibody:

Bullous Pemphigoid
Anti-epidermal basement membrane
Autoantibody:

Type I Diabetes Mellitus
Anti-islet cell
Autoantibody:

Pemphigus
Anti-keratinocyte junction
Autoantibody:

Pernicious Anemia
Anti-intrinsic factor
Anti-parietal cell
Autoantibody:

Microscopic Polyangiitis
p-ANCA
Autoantibody:

Polymyositis
Speckled ANA
20% have anti-Jo-1
Autoantibody:

Progressive Systemic Sclerosis
Anti-Scl 70
Autoantibody:

Sjogren's Syndrome
Anti-SS A (anti-Ro)
Anti-SS B (anti-La)
Autoantibody:

Idiopathic Thrombocytopenic Purpura (adult form)
Anti-structural platelet
Autoantibody:

Vitiligo
Anti-melanocyte
Clinical Triad:

Autoimmune Hemolytic Disease
2 types: warm antibody, cold antibody

Warm:
Severe anemia
Splenomegaly
High MCHC

Cold:
Anemia
Raynaud's syndrome
Acrocyanosis
Clinical Triad:

Bullous Pemphigoid
Bullae
Pruritis
Elderly
Clinical Triad:

Type I Diabetes Mellitus
Hyperglycemia
DKA risk
Infections

Long-term:
Retinopathy
Nephropathy
Atherosclerosis
Clinical Triad:

Pemphigus
Nikolsky's sign (skin sloughs off easily)
Oral and skin erosions
Older patients
Clinical Triad:

Pernicious Anemia
Megaloblastic anemia
Gastritis
B12 deficiency
Clinical Tetrad:

Polyarteritis Nodosa
Fever
Hypertension
Abdominal pain
Renal disease without glomerulonephritis
Clinical Triad:

Microscopic Polyangiitis
Hemoptysis
Hematuria
Palpable purpura

With glomerulonephritis
Clinical Triad:

Polymyositis
Proximal muscle weakness
Elevated muscle enzymes
Elevated myoglobin
Clinical Triad:

Progressive Systemic Sclerosis
Visceral organ fibrosis
Facial tightening
Sclerodactyly
Clinical Triad:

Sjogren's Syndrome
Xerostomia (dry mouth)
Keratoconjuctivitis sicca
Arthritis
Clinical Triad:

Idiopathic Thrombocytopenic Purpura (adult form)
Thrombocytopenia
Petechiae and purpura
Mucosal bleeding
Clinical Triad:

Vitiligo
Hypopigmented areas of skin
White hair in areas of affected skin
Sunburn risk
Clinical Criteria:

Rheumatoid Arthritis
Need 4 for diagnosis

Morning stiffness > 1 hr
Arthritis in 3 or more joints simultaneously
Arthritis in hand joints
Symmetrical arthritis
Rheumatoid nodules
Serum rheumatoid factor
Erosions or bony decalcification identifiable on X-ray
Clinical Triad:

Systemic Lupus Erythematosus (SLE)
Malar rash
Lupus nephropathy
Arthritis
Clinical Pentad:

CREST
Calcinosis
Raynaud's
Esophageal dysmotility
Sclerodactyly
Telangiectasia
Clinical Triad:

Drug Induced Lupus
Arthralgia
Fever
Serositis
Clinical Triad:

Myasthenia Gravis
Post-use episodic muscle weakness
Ptosis
Thymus gland pathologies
Clinical Triad:

Graves' Disease
Symptomatic hypothyroidism
Exophthalmos
Pretibial myxedema
Clinical Triad:

Hashimoto's Thyroiditis
Nontender goiter
Typically female
Hypothyroidism which becomes symptomatic
Clinical Triad:

Wegener's Granulomatosis
Sinusitis
Glomerulonephritis
Lung lesions (cavitary)
Clinical Triad:

Celiac Sprue
Malabsorption (often with diarrhea)
Dermatitis herpetiformis (papular vesicular rash with pruritis and burning, presents symmetrically on body)
Short stature
Clinical Triad:

Primary Biliary Cirrhosis
Pruritis
Female
Jaundice
Autoantibody:

Rheumatoid Arthritis
Anti-IgG
Autoantibody:

Systemic Lupus Erythematosus (SLE)
Anti-nuclear antibody (ANA) for screening
Anti-ds DNA for confirmation
Autoantibody:

Drug Induced Lupus
Anti-histone
Autoantibody:

CREST
Anti-centromere
Autoantibody:

Myasthenia Gravis
Anti-ACh receptor
Autoantibody:

Graves' Disease
Anti-TSH receptor
Autoantibody:

Hashimoto's Thyroiditis
Anti-microsomal
Autoantibody:

Wegener's Granulomatosis
Anti-neutrophil cytoplasm (ANCA)
Autoantibody:

Celiac Sprue
Anti-gliadin
Autoantibody:

Goodpasture's Syndrome
Anti-glomerular basement membrane (anti-GBM)
Autoantibody:

Primary Biliary Cirrhosis
Anti-mitochondrial
What is the mediator of Type I Hypersensitivity?
IgE
What are typical allergens/triggers of Type I Hypersensitivity?
Pollens
Drugs
Foods
Insect Venom
Animal Dander
What mediates Type II Hypersensitivity?
Antibodies

Cytotoxic
What are the triggers for Type II Hypersensitivity?
Blood and Rh antigens
Drugs that attach to RBC membranes (penicillin, quinidine)
Drugs that attach to platelet membranes (quinine)
Drugs that change host tissues (hydralazine)
Infectious agents - molecular mimicry (rheumatic fever)
Autoimmunity
What are some examples of Type II Hypersensitivity reactions?
Autoimmunity
Transfusion reactions
Erythroblastosis fetalis
Theumatic fever
Drug-induced lupus
What mediates Type III Hypersensitivity?
Immune complex deposition
What are the triggers for Type III Hypersensitivity?
Drugs
Vaccines*
Inhaled antigens (ex: fungus)
What are examples of Type III Hypersensitivity reactions?
Arthus reacition
Serum sickness
What mediates Type IV Hypersensitivity?
Cell-mediated
What are examples of Type I Hypersensitivity reactions?
Allergic rhinitis
Systemic anaphylaxis
Eczema
Hives
What are the triggers for Type IV Hypersensitivity?
Delayed type:
Poison ivy/oak
Nickel
Soaps
Mycobacterial infection
Transplanted tissue

T-cell mediated Cytotoxicity:
Transplanted cells
Virus-infected cells/tissue
Tumor cells
What are examples of Type IV Hypersensitivity reactions?
Delayed type:
Contact dermatitis
Acute graft rejection
Positive PPD skin test

T-cell mediated Cytotoxicity:
Acute graft rejection
Viral infection
Neoplasia
What makes Type IV Hypersensitivity unique from the other types of hypersensitivity?
No antibodies involved

Type I, II, III all involve antibodies in some way
Mechanism of:

Hyperacute Transplant Rejection
Type II Hypersensitivity

Preformed antibodies bind to antigen on tissues

Onset: minutes to hours
Mechanism of:

Acute Transplant Rejection
Type IV Hypersensitivity - T cell mediated cytotoxicity

Memory T cells recognize antigen
CD8 T cells destroy graft

Onset: days to months
Mechanism of:

Chronic Transplant Rejection
Type II and III Hypersensitivity

Antibodies develop over time and damage graft vasculature

Onset: months to years
Mechanism of:

Graft vs. Host
Type IV Hypersensitivity - T cell mediated cytotoxicity

T cells in transplanted tissue attack host

Onset: days to weeks
Oncogene:

c-myc
Burkitt lymphoma
Oncogene:

c-abl
Chronic myelogenous leukemia (CML)
Oncogene:

ras
Colon carcinoma
Tumor Suppressor Gene:

BRCA-1
Breast cancer
Ovarian cancer
Tumor Suppressor Gene:

p53
Breast cancer
Colon cancer
Lung cancer

(carcinomas)
What is the difference between an onocogene and a tumor suppressor gene, with regard to contributing to the development of cancer?
Oncogene: when ACTIVE causes uncontrolled cell division

Tumor suppressor: when MUTATED or LOST allows uncontrolled cell division
Tumor Marker:

Carcinoembryonic Antigen (CEA)
Adenocarcinomas
Tumor Marker:

Alpha-fetoprotein (AFP)
High:
Hepatoma
Multiple gestation
Neural tube defects (found in mother during pregnancy)
Yolk sac tumor
Endodermal sinus disease

Low:
Down's syndrome
Tumor Marker:

Prostate Specific Antigen (PSA)
Prostate cancer
Tumor Marker:

Acid Phosphatase
Prostate cancer
Tumor Marker:

Alkaline Phosphatase
Diagnose:
Non-neoplastic bone disease
Non-neoplastic disease of biliary system

Track:
Bone cancers
Renal cell carcinoma

Normally produced in four places:
Bone
Kidney
Placenta
Biliary system
Tumor Marker:

5'-HIAA (5'-hydroxyindole acetic acid)
Carcinoid
Tumor Marker:

CA 19-9
Colon cancer
Pancreatic cancer
Breast cancer
Tumor Marker:

CA 125
Ovarian cancer
Tumor Marker:

CD 25
Hairy cell leukemia
Adult T-cell lymphoma
Tumor Marker:

CD 30
Hodgkin's disease
Tumor Marker:

Neuron-specific Enolase
Small cell lung cancer
Neuroblastoma
Tumor Marker:

Human Chorionic Gonadotropin (beta-hCG)
Pregnancy
Gestational trophoblastic disease (hydatidiform mole)
Choriocarcinoma
Most likely sites of metastasis:

Breast Cancer
Bone > Brain
Most likely sites of metastasis:

Lung Cancer
Brain > Bone
Key Facts:

Autosomal Dominant Inheritance
Never skips generations
Key Facts:

X-Linked Dominant Inheritance
No male to male transmission
Never skips generations
Key Facts:

X-Linked Recessive Inheritance
No male to male transmission
Key Facts:

Mitochondrial Inheritance
Passed from mother to ALL children
Never passed from father to children

Often variable penetrance
Key Facts:

De Novo Mutation (Inheritance)
Both parents healthy, but one progeny has mutation/disease

Will probably follow one of normal inheritance patterns in the mutated progeny's offspring
What are the questions to ask when determining inheritance pattern?
1. Are any generations skipped? If yes, not dominant.

2. Is there any male to male transmission? If yes, not X-linked.
Inheritance Pattern:

Hyperphosphatemic Rickets
X-Linked dominant

Inherited vitamin D resistance
Bowed legs
Inheritance Pattern:

Incontinentia Pigmenti
X-Linked dominant

Mini-teeth
Patchy alopecia
Inheritance Pattern:

Leber's Optic Neuropathy
Mitochondrial

Bilateral blindness with onset sometime after 15 years of age (variable penetrance)
Cystic Fibrosis
Most common lethal genetic disease of Caucasians

Autosomal Recessive inheritance

Mutation in CFTR gene - defect in chloride transmembrane movement in epithelial cells

Clinical Findings:
Recurrent respiratory infections (Staph aureus first 6 mos, Pseudomonas aeruginosa 6 mos and older)
Meconium ileus
Viscous mucus
High NaCl in sweat and tears (positive sweat test)
Chronic pancreatitis
Cholelithiasis
Malnutrition due to poor bowel function
Phenylketonuria
Autosomal Recessive inheritance

Unable to metabolize amino acid Phenylalanine
Buildup of Phenylalanine brakdown products
Inability to make melanin, norepinephrine, dopamine (lack phenylalanine hydroxylase)

Neurotoxicity from phenylalanine breakdown products (phenylketones)
Lighter complexion due to lack of melanin
Mental retardation (preventable if stop intake of phenylalanine)
Albinism
Autosomal Recessive inheritance

Inability to make melanin
Lack tyrosinase (convert tyrosine to melanin)
Alpha-1 Antitrypsin Deficiency
Autosomal Recessive inheritance

Loss of inhibition of elastase
Liver destruction (liver makes alpha-1 antitrypsin but can't release it)

Primarily destroys elastic tissue in lung
Emphysema
Thalassemias, Sickle Cell Anemia
Autosomal Recessive inheritance

Abnormally structured hemoglobin resulting in RBC defects that cause RBC destruction

Microcytic anemia
Glycogen Storage Diseases
vonGierke disease
Pompe disease
McArdle disease

Autosomal Recessive inheritance

Inability to utilize glycogen stores normally
Mucopolysaccharidoses
Lysosomal storage disease
Unable to metabolize GAGs (component of connective tissue)

May or may not cause mental retardation or corneal clouding
Gargoyle-like facies

Hurler
Scheie
Autosomal Recessive inheritance

Hunter
X-Linked Recessive inheritance
Sphingolipidoses
Lysosomal storage disease
Unable to metabolize sphingolipids (molecules involved with myelin and CNS)

Niemann-Pick
Gaucher's
Krabbe's
Tay-Sachs
Metachromatic dystrophy
Autosomal Recessive inheritance
Cause serious CNS disorders

Fabry
X-linked Recessive inheritance
Does not cause serious CNS disorders