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238 Cards in this Set

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How do many antiviral agents interfere with viral DNA synthesis or transcription?
Many of the drugs are phosphorylated into triphosphorylated form
This form mimics nucleotide triphosphates
The drug is incorporated into synthesis process and blocks further action
MOA:

Amantidine
Antiviral

Impairs uncoating of virus (removal of capsid to allow viral nucleic acid to be released into cell)

Binds to M2 matrix protein of influenza A
Only effective within 48 hours of symptom onset (similar drug: rimantadine)

No longer recommended for use: resistance
MOA:

Interferon
Antiviral

Induces host cell responses to inhibit RNA translation
Induces MHC-1 expression

DOC for chronic HBV and HCV
Used to treat hairy cell leukemia

Pegylated form most common (does not require daily dosing)
MOA:

Ribavirin
Antiviral

Phosphorylated to becom ribavirin triphosphate
Mimics GTP (guanosine triphosphate)
Incorporated into transcription, eventually blocks viral mRNA synthesis

DOC for chronic HCV
Standard of therapy for HCV: Pegylated interferon alpha PLUS ribavirin
MOA:

Acyclovir
Antiviral

Phosphorylated to acyclovir triphosphate
Mimics GTP
Is incorporated into DNA and causes inhibition of DNA polymerase
Also causes premature DNA chain termination

Requires viral thymidine kinase for phosphorylation (only found in select viruses)
Selective for HSV-1, HSV-2, VZV (varicella zoster), EBV (Epstein Barr)

DOC for HSV-1 and HSV-2

Penetrates BBB

Similar drug: Valacyclovir (longer half life, less frequent dosing)
MOA:

Vidarabine
Antiviral

Phosophorylated to imitate ATP
Incorporated into DNA, inhibits synthesis

Treats all herpes group viruses
Especially herpes encephalitis, VZV (varicella zoster) in immunocompromised patients

In ointment form, second line (to trifluridine) for herpes keratitis
MOA:

Ganciclovir
Antiviral

Phosphorylated to mimic GTP
Incorporated into DNA, inhibits DNA polymerase, causes premature DNA chain termination

Similar to Acyclovir but does NOT require viral thymidine kinase

DOC for CMV retinitis (in combination with Valganciclovir)

Side effect: bone marrow suppression (causes neutropenia or aplastic anemia)
MOA:

AZT (Zidovudine)
Antiviral (anti-retroviral - NRTI [nucleoside reverse transcriptase inhibitor])

Triphosphorylated by human thymidine kinase
Mimics TTP
Incorporated into DNA and inhibits synthesis

Good BBB penetration

Treats HIV
NRTIs (Nucleoside Reverse Transcriptase Inhibitors)
Anti-retroviral

AZT (Zidovudine)
Didanosine (ddl)
Stavudine (d4T)
Lamivudine (3TC)
MOA:

Protease Inhibitors
Antiviral

Inhibit cleavage of "giant" protein (gag-pol-env)
Cleavage required by HIV to have functional components of the protein

Used for HIV

Saquinavir
Ritonavir
Indinavir
Nelfinavir
Fosamprenavir
MOA:

NNRTIs (Non-Nucleoside Reverse Transcriptase Inhibitors)
Antiviral

Directly inhibit reverse transcriptase

Used for HIV

Nevirapine
Delavirdine
Efavirenz
MOA:

Fusion Inhibitors
Antiviral

Prevent fusion between HIV virion and cell
Binds to gp41 and prevents fustion with cell membrane

Enfuvirtide

Increases risk for bacterial pneumonia
Most common side effects are insomnia, headache, nausea
Severe hypersensitivity reactions possible
MOA:

Integrase Inhibitors
Antiviral

Inhibit HIV viral integrase enzyme
Prevents integration and insertion of HIV DNA into human DNA

Raltegravir
MOA:

Chemokine Co-Receptor Antagonists (CCR5 Antagonists)
Antiviral

Block CCR5 co-receptor on WBCs targeted by HIV
Prevents entry of virus into cell

Used in CCR5-topic HIV-1 (R5 virus) that has demonstrated multi-drug resistance

Maraviroc

Hepatotoxic
MOA:

Neuraminidase Inhibitors
Antiviral

Inhibit influenza virus neuraminidase

Used for prophylaxis of influenza A and B in close contacts with infected persons
Used to attenuate early disease

Zanamivir (not for use in lung disease - causes bronchospasm)
Oseltamivir
MOA:

Foscarnet
Antiviral

Direct inhibitor of both DNA polymerase and reverse transcriptase

Alternative to ganciclovir for CMV
Used for ganciclovir-resistant CMV
Used for ganciclovir and acyclovir-resistant VZV and HSV

May be useful against HIV but not part of HIV-HAART regimen

Nephrotoxic
MOA:

Valganciclovir
Antiviral

Used in combination with ganciclovir for CMV retinitis

May cause myelosuppression

Contraindicated with ganciclovir allergy
MOA:

Trifluridine
(Trifluorothymidine)
Antiviral

Mimics TTP
Incorporated into DNA and inhibit synthesis
Does not require viral thymidine kinase

Active against HSV including emerging thymidine kinase deficient mutants resistant to acyclovir

DOC for herpes keratitis (solution form)
MOA:

Cidofovir
Antiviral

Alternative treatment for CMV retinitis
DOC for smallpox, severe adenovirus infections

Extremely nephrotoxic
Can cause Fanconi syndrome at low doses (proximal convoluted tubule destruction)
Generally administered with Probenecid to minimize dose/maximize systemic antiviral effect

Suppresses viral replication by selective inhibition of viral DNA synthesis

Acyclic nucloside phophonate - functions without being phosphorylated (already has mimicry)

Very teratogenic
Key Features:

Osteogenesis Imperfecta
Congenital

Disorder of collagen synthesis

Fractures
Blue, thin sclera
Key Features:

Osteopetrosis
Congenital

Increased density
Brittle bones
Facial distortion due to bone overgrowth
Key Features:

Achondroplasia
Congenital
Autosomal dominant

Defective cartilage synthesis
Decreased epiphyseal formatoin
Short limbs, normal sized head and torso
Key Features:

Osteoporosis
Acquired

Thinned cortical bone
Enlarged medullary cavity

Normal Ca, phosphate
Normal alkaline phosphatase

Decreased bone mass
Estrogen deficiency
Immobilization
Cushing's syndrome
Key Features:

Osteomalacia
Acquired

Diffuse radiolucency

Low Ca, phosphate
High alkaline phosphatase

Impaired mineralization
Lack of vitamin D
Chronic renal insufficiency
Key Features:

Paget's Disease
Acquired

Bones enlarged and radiolucent

Extremely high alkaline phosphatase

Excessive bone resorption with replacement
Gradual enlargement and deformation of bones (osteitis deformans)
Increased osteoclast and osteoblast activity

Characteristic mosaic pattern of bone on X-ray
Hyaline Cartilage
Type II collagen

Found in:
Joints
Developing bones
Trachea/larynx
Nose
Elastic Cartilage
Elastin

Found in:
Ear
Fibrocartilage
Type I collagen

Found in:
Intervertebral disks
Menisci
Osteochondroma
Benign tumor of cartilage

Developmental defect
Exostosis at metaphyseal projections
Enchondroma
Benign tumor of cartilage

May develop into chondrosarcoma (malignant)
Cartilage within bone
Chondroblastoma
Benign tumor of cartilage

Femur, tibia, humerus epiphysis
Chondrosarcoma
Malignant tumor of cartilage

Spine, pelvic bones
Slower growing than osteosarcoma
Osteoma
Benign bone tumor

Skull
Osteoid Osteoma
Benign bone tumor

Painful
Tibia or femur (diaphysis)
Osteoblastoma
Benign bone tumor

Like osteoid osteoma
Larger but painless
May be malignant
Osteosarcoma
Highly malignant bone tumor

Metaphysis of long bone (knee)
Codman's triangle
Ewing's Sarcoma
Malignant bone tumor

Very aggressive
Young males
Pelvis, long bones
Within marrow cavity
"Onion skin" appearance
What is Codman's triangle?
Triangular area of new subperiostal that is created when a tumor raises the periosteum from the bone

Usually found in osteosarcoma
Duchenne Muscular Dystrophy
X linked
Absent dystrophin protein

Most severe of muscular dystrophies
Pelvic girdle weakness
Pseudohypertrophy of calves (fatty and fibrous infiltration of calf muscles)
Gower's sign
Usually boys age 3-7
Proximal muscle weakness with waddling gait
Increased serum CPK
Becker Muscular Dystrophy
X linked
Abnormal dystrophin protein

Less severe than Duchenne
May walk until age 20-25
Limb Girdle Muscular Dystrophy
Autosomal recessive

Late onset
Facioscapulohumeral Muscular Dystrophy
Autosomal dominant

Late onset
Myotonic Muscular Dystrophy
Autosomal dominant

Late onset

Distal limb involvement
Inability to voluntarily relax muscle
What is Gower's Sign?
When trying to stand up, child uses its hands to "climb" up his/her own body
Neural Tube Brain Tumors
Astrocytoma
Glioblastoma
Medulloblastoma
Oligodendroblastoma
Astrocytoma
Neural tube

Slow growing
M > F
Glioblastoma
Neural tube

Always fatal
M > F
Medulloblastoma
Neural tube

Children
M > F
Oligodendroblastoma
Neural tube

Rare
M = F
Slow growing
Seizures
Neural Crest Brain Tumors
Meningioma
Schwannoma
Neurofibroma
Meningioma
Neural crest

From arachnoid
Benign
F > M
Whorling pattern
Psammoma bodies
Schwannoma
Neural crest

Acoustic neuroma
F > M
Associated with Von Recklinghausen's
Neurofibroma
Neural crest

Fibroblasts and Schwann cells
Benign
Associated with Von Recklinghausen's
Ectoderm Brain Tumors
Craniopharyngioma
Pituitary Adenoma
Craniopharyngioma
Ectoderm

Most common supratentorial tumor in children
Compresses optic nerve
Pituitary Adenoma
Ectoderm

60% prolactin (chromophobe)
10% growth hormone (eosinophil)
10% ACTH (basophil)
Mesoderm Brain Tumors
Lymphoma
Lipoma
Hemangioblastoma
Lymphoma
Mesoderm

B Cells
Periventricular
Lipoma
Mesoderm

Egg shell appearance
What is the most common degenerative disease of the CNS?
Alzheimer's
Alzheimer's Disease
Diffuse cortical atrophy
Senile plaques (beta-amyloid protein)
Neurofibrillary tangles (cytoplasmic deposit of tau protein)

Most common degenerative disease of CNS
Pick's Disease
CNS degenerative disease

Lobar atrophy
Mainly frontal and temporal
Parkinson's Disease
CNS degenerative disease

Bradykinesia, rigidity, resting tremor
Dopamine depletion (caudate, putamen)
Lewy bodies (spherical inclusions in melanin-depleted neurons of substantia nigra)
ALS
CNS degenerative disease

Rapidly progressive
Degeneration of corticospinal tract (UMN)
Degeneration of alpha-motorneurons (LMN)
Huntington's Disease
CNS degenerative disease

Chorea, athetoid movements
Atrophy of caudate, putamen, frontal cortex

Autosomal dominant
Friedreich's Ataxia
CNS degenerative disease

Pes cavus
Loss of proprioception
Tremors
Babinski reflex
Spinal cord atrophy (spinocerebellar, corticospinal, posterior columns)

Autosomal recessive
Upper motor neuron lesions cause:
Spasticity
Increased tendon reflexes
Lower motor neuron lesions cause:
Paralysis
Fasciculations
Absent tendon reflexes
Multiple Sclerosis
Demyelinating disease of CNS

Onset at age 20-40
Associated with cool, temperate climate
Oligoclonal bands on CSF electrophoresis (multiple monoclonal gamma globulins - characteristic but not entirely specific)
Devic's Disease
Demyelinating disease

Like MS but limited to spinal cord and optic nerve
Guillan-Barre Syndrome
Demyelinating disease of PNS

Mainly peripheral motor nerves
Autoimmune (often follows viral infection)
Adrenoleukodystrophy
Demyelinating disease

Accumulation of long chain cholesterols
Blindness, ataxia
Latent adrenal insufficiency

X linked
Schilder's Disease
Demyelinating disease

Focal to brain
Children

Visual, auditory, motor defects
Variant of adrenoleukodystrophy
Hyperfunction of Anterior Pituitary:
Eosinophile Cells
Prolactin:
Male: decreased libido, impotence
Female: galactorrhea, amenorrhea, infertility

Growth Hormone:
Prepubertal: giantism
Adults: acromegaly
Hyperfunction of Anterior Pituitary:
Basophile Cells
ACTH:
Cushing's disease
Sheehan's Syndrome
Pituitary hypofunction
Panhypopituitarism

Caused by ischemic necrosis (often postpartum)

Hypothyroidism
Hypogonadism
Hypoadrenalism
Dwarfism
Pituitary hypofunction

Growth hormone deficiency or lack of receptors
Eunuchoid Pituitary Hypofunction
Hypogonadism
Primary amenorrhea

Gonadotropin deficiency (common)
What are the two parts of the adrenal gland? What do they produce?
Cortex - Steroids
Medulla - Epinephrine, Norepinephrine
Adrenal Adenoma
Cortex

Most do not produce steroids

Conn (increased mineralocorticoids)
Cushing (increased glucocorticoids)
Virilization (increased androgens)
Adrenal Carcinoma
Cortex

Much rarer than adenomas
Usually produce hormones
Pheochromocytoma
Adrenal medulla

10% extra-adrenal
10% bilateral
10% malignant
Adrenal Neuroblastoma
Common in children under 5

From medulla or sympathetic chain ganglia
Conn Syndrome
Adrenal adenoma (cortex)

Increased mineralocorticoids

Hypernatremia
Hypervolemia
High BP

Potassium loss -> muscle weakness
Cushing's Syndrome
Adrenal adenoma (cortex)

"Moon face"
"Buffalo hump"
Truncal obesity
Skin striae
Osteoporosis
Low glucose tolerance
What are the three zones of the adrenal cortex? What do they produce?
Zona Glomerulosa - Mineralocorticoids

Zona Fasciculata - Glucocorticoids

Zona Reticularis - Androgens
What are the two cell types in the thyroid gland? What do they produce?
Follicle cells - T3/T4

Parafollicular C-cells - Calcitonin
Graves' Disease
Hyperthyroidism
Diffuse Toxic Goiter

Lymphocytes
Small follicles
Little colloid
Plummer's Disease
Hyperthyroidism
Nodular Toxic Goiter

Hyperplasia
Hypertrophy
Colloid accumulation
Diffuse Simple Goiter
Hypothyroidism
Iodine deficiency

Hyperplasia
Hypertrophy
Hashimoto's Thyroiditis
Hypothyroidism

Lymphocytes
Plasma cells
Atrophic follicles
Little colloid
Riedel's Thyroiditis
Hypothyroidism

Fibrous replacement
De Quervain's Thyroiditis
Euthyroid

Viral
Leakage of colloid
Granulomas
Sick Euthyroid Syndrome
Low T3/T4 but no clinical signs of hypothyroidism

TSH normal

Caused by severe illness, trauma, stress
Follicular Thyroid Adenoma
Benign
Very common
Most are cold nodules
Papillary Thyroid Cancer
Malignant
Younger patients
Associated with radiation exposure
Psammoma bodies

More common than follicular carcinoma
Follicular Thyroid Cancer
Malignant
Adenomatous pattern

More aggressive than papillary carcinoma
Anaplastic Thyroid Cancer
Malignant
Undifferentiated
Poor prognosis
Medullary Thyroid Cancer
Malignant
Parafollicular (C-cells)
Often associated with MEN type II
What are the parathyroid glands derived from?
3rd and 4th pharyngeal pouches
What do parathyroids produce?
PTH (parathyroid hormone)

Acts on bone osteoclasts to mobilize calcium
Causes:

Hyperparathyroidism
Primary - adenoma (most common)

Secondary - chronic renal failure, vitamin D deficiency
Causes:

Hypoparathyroidism
Thyroidectomy (most common)
DiGeorge's Syndrome

PTH low
Calcium low
Causes:

Pseudohypoparathyroidism
Receptor defect

Short stature
Short metacarpal bones

PTH high
Calcium low
Pseudopseudohypoparathyroidism
Same physical appearance as in pseudohypoparathyroidism

PTH normal
Calcium normal
Renal Osteodystrophy
Chronic renal failure leads to:
Decreased phosphate excretion
Phosphate binds ionized calcium in serum
Hypocalcemia
Increased PTH
Bone demineralization

TX: Aluminum (to bind phosphate)
What is the most common endocrine disease?
Diabetes Mellitus
IDDM
Type I Diabetes Mellitus
Primary diabetes
Less common

Juvenile onset
Prone to ketoacidosis
Possible viral etiology?
Weak genetic predisposition (HLA DR3, DR4)

Auto-immune - anti-islet cell antibodies
Decreased number of beta islet cells
NIDDM
Type II Diabetes Mellitus
Primary diabetes
Very common

Adult onset
Not prone to ketoacidosis
Strong genetic predisposition

Inadequate insulin secretion
Obesity, insulin resistance
Hyalinization of islet cells
Maturity Onset Diabetes of the Young
Primary diabetes
Rare

Juvenile onset
Glucokinase defect (glucose sensor)
Diabetes Mellitus associated with Hemochromatosis
Secondary diabetes

"Bronze diabetes"
Diabetes Mellitus associated with Chronic Pancreatitis, Pancreas Carcinoma
Secondary diabetes

Islet cell destruction due to associated disease causes diabetes
Gestational Diabetes
1-3% of women

Induces excessive fetal insulin secretion
Increases risk of birth trauma (increased fetal weight)

Glucose tolerance usually returns to normal after birth
30% of women will develop overt DM within 5 years
What is MEN?
Multiple endocrine neoplasia

Autosomal dominant
Inherited disorder with variable penetrance

Type 1 - due to loss of tumor suppressor gene
Neoplasia arises when second (healthy) allele mutates
MEN Type 1
Adrenal cortex

Pituitary
Parathyroid
Pancreas (gastrinoma)

"pity-para-pan"

Clinical presentations:
Primary hyperparathyroidism (90%) -> hypercalcemia
Gastrin (70%) -> Zollinger-Ellison Syndrome -> peptic ulcers
Pituitary tumors (60%) -> visual disturbances (sometimes also produce GH -> acromegaly)
MEN Type 2A
Adrenal medulla

Thyroid medulla
Parathyroid

"para-medullary-medulla"

Clinical presentations:
Medullary carcinoma of thyroid (bilateral) (100%) -> early diagnosis is essential
Benign pheochromocytoma (bilateral) (50%) -> hypertensive crisis (headache, sweating, palpitations)
Primary hyperparathyroidism (20%) -> hypercalcemia
MEN Type 2B
Adrenal medulla

Thyroid medulla
Mucosal neuromas
Marfanoid features
What is the most common cancer in the US?
Skin cancer

Directly related to exposure

80% basal cell carcinomas with very low metastatic potential
Seborrheic Keratosis
Benign skin tumor

Brownish/gray
Scaly
Greasy
Keratocanthoma
Benign skin tumor

Rapidly growing pink papules
Looks like squamous cell carcinoma but is benign
Actinic Keratosis
Benign skin tumor

Crusty red papule
Premalignant
Basal Cell Skin Carcinoma
Malignant skin tumor

Pearly gray papule
Squamous Cell Skin Carcinoma
Malignant skin tumor

Erythematous, scaly, or oozing ulcer
Bowen's disease - squamous carcinoma in situ
Skin Melanoma
Malignant skin tumor

Brown, black, red, white, purple
Irregular borders

Lentigo maligna - grows horizontally
Nodular melanoma - grows vertically

"ABC":
Asymmetric lesion
Borders irregular
Color variations
Diameter increasing
Pemphigus
Vesicles on mucosa
Autoantibodies against intercellular junctions of keratinocytes
Pemphigoid
Like pemphigus but larger bullae on abdomen and groin
Impetigo
Honey colored crust
Superficial skin infection
Staphylococcus or beta-hemolytic Streptococci
Pityriasis
Viral cause?
Herald patch that then spreads along flexural lines
Rosacea
Large red nose
Pemphigus
Vesicles on mucosa
Autoantibodies against intercellular junctions of keratinocytes
Pemphigoid
Like pemphigus but larger bullae on abdomen and groin
Impetigo
Honey colored crust
Superficial skin infection
Staphylococcus or beta-hemolytic Streptococci
Pityriasis
Viral cause?
Herald patch that then spreads along flexural lines
Rosacea
Large red nose
Xanthoma
Hyperlipidemia
Foamy histocytes
Capillary Hemangioma
"Salmon patches" and stork bites
Spontateously regress

Strawberry hemangiomas
Initially grow, later regress
Cavernous Hemangioma
Port wine stain
Assosciated with Sturge-Weber
Does not resolve spontaneously
Cafe-au-Lait Spots
Associated with Von Neurofibromatosis
Vitiligo
Irregular depigmentation
Pathology Associated With Toxin:

Cadmium
Honeycomb pneumonia
Pathology Associated With Toxin:

Cobalt
Cardiomyopathy
Pathology Associated With Toxin:

Chromium
Lung cancer
Pathology Associated With Toxin:

Lead
Inhibits heme synthesis
Renal tubular acidosis
Pathology Associated With Toxin:

Mercury
Neurotoxic (Minamata disease)
Proximal tubular necrosis
Pathology Associated With Toxin:

Arsenic
Lung cancer
Pathology Associated With Toxin:

Asbestos
Mesothelioma
Pathology Associated With Toxin:

Aromatic Amines
Bladder cancer
Pathology Associated With Toxin:

Benzene
Leukemia
Pathology Associated With Toxin:

Vinyl Chloride
Liver angiosarcoma
Pathology Associated With Toxin:

Alpha-Amanitin
Fulminant hepatitis
Pathology Associated With Toxin:

Carbon Monoxide (CO)
Forms carboxyhemoglobin

Do not confuse with methemoglobin, which contains oxidized Fe+3
Pathology Associated With Toxin:

Cyanide
Inhibits mitochondrial cytochromes
Loss of O2 utilization
Microscopic Findings:

Amyloid
Birefringence
Microscopic Findings:

Reed-Sternberg Cells
Hodgkin's Disease
Microscopic Findings:

Barrett's Esophagus
Metaplasia
Microscopic Findings:

Granulomas
Caseating: TB

Non-Caseating: foreign body
Microscopic Findings:

Teratoma
Skin, teeth, neural tissue, etc
Microscopic Findings:

Kidney Immunofluoresence
Linear: Goodpasture's

Granular: Membranous GN

Mesangial: IgA Nephropathy
Microscopic Findings:

Alzheimer's Disease
Neurofibrillary tangles
Plaques
Microscopic Findings:

Parkinson's Disease
Depigmentation of substantia nigra
What structures comprise the bony thorax?
Thoracic spine
Ribs
Sternum
Name the facets of the thoracic vertebrae and their articulations:
Costal facets - Rib heads and tubercles (same number rib/vertebra)
Articular facets (Zygophphyseal facets), superior and inferior - Superior and inferior vertebrae
What is the "rule of threes" in the thoracic spine?
T1-T3 = transverse process located on same horizontal plane as spinous process of given vertebra

T4-T6 = transverse process located halfway between that vertebra's spinous process and the spinous process of the vertebra above it

T7-T9 = transverse process located on horizontal plane corresponding with spinous process of vertabra directly above it

T10 = T7-T9
T11 = T4-6
T12 = T1-T3
What are the features of typical ribs? Which are the typical ribs?
Head
Neck
Tubercle
Angle
Shaft
(Must have all 5)

Ribs 3-10
What are the features of atypical ribs? Which are the atypical ribs and why?
Any rib that does not have all five features of a typical rib

Rib 1 - no angle, head only articulates with T1 (most articulate with two vertebrae)
Rib 2 - Extra tuberosity on shaft
Ribs 11, 12 - No neck or tubercle, head that only articulates with one corresponding vertebra

Rib 10 sometimes considered atypical - head only articulates with corresponding vertebra
What are true ribs?
Connected directly to sternum by costal cartilage

Ribs 1-7
What are false ribs?
Not directly connected to sternum

Ribs 8-10 - connect by costal cartilage to rib superior to them

Ribs 11, 12 also false ribs (although classified as floating ribs) - do not connect to sternum at all
What are floating ribs?
Do not connect to sternum at all

Ribs 11,12
What is the broadest and most curved rib?
Rib 1
What are the functions of the ribs?
Motion
Support
Protection
What is the primary motion of the thoracic spine?
Rotation

Order of ease for thoracic motion:
Rotation > Flexion/Extension > sidebending
What is special about the motion of T11 and T12?
More akin to lumbar vertebrae

Order of ease:
Flexion/Extension > Sidebending > Rotation
What are the three types of rib motion?
Pump handle (ribs 1-5)
Bucket handle (ribs 6-10)
Caliper (ribs 11, 12)
What are the muscles of inspiration?
Primary:
Diaphragm
Intercostals (external, internal, innermost, subcostal)

Secondary:
Scalenes
Pectoralis minor
Latissimus dorsi
Quadratus lumborum
Serratus anterior and posterior
Explain the actions of the diaphragm in respiration:
Contracts with inspiration
Relaxes with expiration

Contraction/relaxation causes pump-like action to aid in return of lymph and venous blood back to thorax

Attachments:
Ribs 6-12 bilaterally
Bodies and intervertebral discs of L1-L3
Xyphoid process

Innervation: phrenic nerve (originates from C3-C5 nerve roots)
Explain the use of the intercostal muscles in respiration:
Lift ribs with inhalation
Prevent retractions during inspiration
Inhalation Somatic Dysfunction (Ribs)
Exhalation restriction

Engaged as if in inhalation ("stuck up")

Key rib: lowest in group (bottom)
Exhalation Somatic Dysfunction (Ribs)
Inhalation restriction

Engaged as if in exhalation ("stuck down")

Key rib: highest in group (top)
Thoracic level of sternal notch:
T2
Thoracic level of spine of scapula:
T3
Thoracic level of sternal angle (angle of Lous):
T4
Thoracic level of inferior angle of scapula:
T7
What cell type does HIV destroy?
CD4 T cells
What are the two types of HIV?
Serotypes:
HIV-1 (predominant)
HIV-2 (mainly in Africa)
How is HIV transmitted?
Blood
Semen
Vaginal secretions
Breast milk
What are the three stages of HIV infection?
Acute:
3-4 wks to develop antibodies (may take months)
Symptomatic with "generalized viral symptoms"

Latent Period:
Asymptomatic
NOT latent in reproduction of HIV, but in symptoms

Advanced Symptomatic Infection (AIDS):
Defined by clinical parameters
What are the clinical parameters to define AIDS?
Positive HIV test PLUS one of the following

1) <200 CD4 T cells/uL

2)AIDS defining opportunistic infections (Pneumocystis pneumonia, Toxoplasmosis, CMV retinitis, Mycobacterium avium complex, progressive multifocal leukoencephalopathy, cryptococcal meningitis)

3) AIDS associated malignancies (Kaposi's sarcoma, brain lymphoma, invasive cervical cancer, some non-Hodgkin's lymphomas)

4) HIV complicating infections (HIV dementia/encephalopathy, extrapulmonary TB, chronic isosporiasis or cryptosporidosis, disseminated histoplasmosis, chronic or pulmonary HSV, disseminated coccidiomycosis, esophageal or respiratory candidiasis)
What are direct effects/complications of HIV infection?
Fever
Weight loss
Cachexia
Night sweats
What are the two methods of clot formation?
Platelet activation and aggregation

Clotting cascade activation
What does a bleeding time test?
Platelet function
What does a PT (prothrombin time) test?
Extrinsic and common pathways of clotting cascade

Factors I, II, V, VII
What does a PTT (partial thromboplastin time) test?
Intrinsic and common pathways of clotting cascade

All factors except VII, XIII
What does TT (thrombin time) test?
Common pathway of clotting cascade

Factors I, II
Von Willebrand Disease
Deficiency of Von Willebrand Factor
Also causes factor VIII functional deficiency

Autosomal dominant

Tx: VWF or humate (purified factor VIII)
May include desmopressin (DDAVP) to release factor VIII from endothelial cells

Signs and Symptoms:
Bleeding from small cuts
Easy bruising
Increased menstrual bleeding
Increased PTT AND bleeding time
Hemophilia A
Lack of factor VIII

Tx: factor VIII

X-linked recessive
Excessive bleeding
Increased PTT
Normal PT and bleeding time
Hemophilia B
Christmas Disease

Lack of factor IX

Tx: factor IX

X-linked recessive
Excessive bleeding
Increased PTT
Normal PT and bleeding time
Vitamin K Deficiency
Results in non-functional factors II, VII, IX, X (need vitamin K to be gamma carboxylated to become activated)

Excessive bleeding

May be due to:
Fat malabsorption - Vit K is fat soluble (Cystic fibrosis, chronic pancreatitis)
Antibiotics (long term or high dose) - destroy gut flora that provide Vit K
Newborns - lack gut flora
Coumadin/Warfarin - prevent vitamin K activation of factors
Disseminated Intravascular Coagulation (DIC)
Coagulation within blood vessel lumens follwed by mucosal bleeding

Disorder of spontaneous activation of coagulation cascade
Results in intravascular coagulation, organ ischemia, consumption of clotting factors to yield mucosal bleeding
May be fatal

May be initiated by:
Bacterial endotoxins
Presence of dead tissue
Certain forms of acute myelogenous leukemia

Initially prolonged PTT with increased d-dimer, then prolonged PT also seen
Idiopathic Thrombocytopenic Purpura( ITP)
Petechiae
Purpura
Mucosal bleeding

Disorder of decreased platelet numbers

Children: acute, post-viral infection, usually self-limiting

Adults: often chronice, anti-structural platelet antibodies

Tx: corticosteroids
Thrombotic Thrombocytopenic Purpura (TTP)
Unknown specific cause
May be associated with autoimmune-induced inhibition of enzyme responsible for destruction/recycling of VWF

Spontaneous platelet aggregation with resulting systemic platelet clot formation and consumption of platelets

FATAL if untreated
Tx: plasmapheresis

Signs and Symptoms:
Severe thrombocytopenia
Schistocytes, helmet cells, triangular RBCs
Evidence of hemolysis (low hemoglobin, high reticulocyte count, polychromasia on blood smear, high LDH [lactate dehydrogenase], ischemic organ damage, fever)
Spherocytosis
Familial spherocytosis, chronic familial icterus, spherocytic anemia

Chronic disease characterized by hemolysis of spheroidal RBCs, anemia, splenomegaly

RBCs are functional, but spleen is insulted and hemolyzes them due to shape
Causes anemia - can be severe
Can be treated by splenectomy

Sphere shaped RBCs due to deficiency in spectrin
G6PD Deficiency
X-linked recessive
More common in blacks

In RBCs, pentose PO4 pathway is sole means of producing NADH
RBCs very sensitive to oxidative damage in G6PD deficiency

RBC lysis occurs on exposure to excess radicals
Fava beans, sulfa drugs, quinine derivatives, many other sources

Most common enzymopathy
Sickle Cell Anemia
Autosomal recessive
Yields HBS instead of normal hemoglobin
Most common in blacks - carrier state confers resistance to malaria

Single amino acid substitution (valine for glutamate) in beta globin chain at 6th amino acid
More prone to crystallization under some circumstances of less than optimal oxygenation - hypoxia, acidosis, dehydration
What is a sickling crisis?
Any sickling event of RBCs
Usually caused by hypoxia, acidosis, dehydration

Results in occlusion of vessels by sickled RBCs

Repeated events result in autosplenectomy (scarring and resulting self-destruction of spleen)
Alpha Thalassemia
Decreased synthesis of alpha globin chains

Homozygosity is lethal

Microcytic anemia and splenomegaly
What is unique about the inheritance of the alpha-thalassemia alleles?
Inherit 2 from each parent

Critical allele, so evolved to make sure that we always have it

1 lost: asymptomatic
2 lost: moderate microcytic anemia
3 lost: severe microcytic anemia
4 lost: lethal
Beta Thalassemia
Decreased synthesis of beta globin chains

Jaundice
Leg ulcers
Splenomegaly

Major = Cooley's anemia (severe microcytic anemia)
Minor (moderate microcytic anemia)
What is Bart's Hemoglobin?
4 gamma globin chains

Found in alpha thalassemia

FATAL
What are the types of autoimmune hemolytic anemia?
Warm agglutinin

Cold agglutinin

Named for temp at which anti-RBCs are most active
Risk factors for warm agglutinin disease:
Drugs (methyldopa, dopa, high dose penicillin or cephalosporin)
Malignancies (leukemia, lymphoma)
SLE
Risk factors for cold agglutinin disease:
Mycoplasma pneumonia
Mononucleosis
Lymphoma

50% are idiopathic
What is the Coombs Test?
Direct:
Mix rabbit antisera to RBC antibodies with patient's RBCs
If RBCs precipitate, RBCs were coated with anti-RBC antibodies
Detects immune-mediated hemolysis
Detects antibodies directly bound to RBCs

Indirect:
Mix patient's plasma with normal RBCs
Anti-RBC antibody presence in plasma will cause RBCs to precipitate
Used to identify free floating antibodies against RBCs
Test of choice for isoimmunization in Rh(-) females
Megaloblastic Anemia
Due to defective DNA synthesis

Leukopenia
Hypersegmented neutrophils
Thrombocytopenia

Caused by:
Vitamin B12 deficiency (also causes neurologic symptoms)
Folate deficiency (no neurologic symptoms)
Antineoplastic drugs
Microbes or drugs that limit folate or B12 availability
What are some causes of Vitamin B12 deficiency?
Diphyllobothrium latum (worm)
Poor diet
Type A gastritis

Megaloblastic anemia AND neurologic symptoms
Plummer-Vinson Anemia
Due to low grade, long term iron deficiency
"Tea and toast" diet

Results in esophageal webs - cause dysphagia for solids (but not for liquids)
What does it mean if dysphagia only affects solids? Both solids and liquids?
Solids only:
Anatomic cause

Solids and liquids:
Neuromuscular cause
Fanconi Anemia
Inability to remove oxygen radicals from bone marrow

Autosomal recessive

Clinical findings:
Microcephaly
Cafe au lait spots
Small or absent thumbs
Deformed or absent radius bones
Recurrent aplastic anemia
High risk for leukemia or lymphoma
Heinz Bodies
Denatured hemoglobin visible within RBCs

G6PD deficiency
Howell-Jolly Bodies
Visible nuclear fragments within RBCs
Appear as basophilic (blue) granules

Indicative that RBCs are leaving marrow while still immature
Basophilic Stippling
Multiple tiny blue dots within RBCs

Lead poisioning
Siderocytes
Pappenheimer bodies

Extra iron in RBCs
Represents iron not bound to hemoglobin
Result of iron overload secondary to deranged bone marrow function (not dietary excess)
Reticulocytes
Immature RBCs
Released early from bone marrow in response to hemorrhage or similar events
Blue lace-like patterns visible within RBCs - remnants of ribosomal RNA
What is neutropenia?
Low number of neutrophils
What are the causes of neutropenia?
Decreased production (bone marrow disease, chemotherapy, HIV infection, VitB12/folate deficiency)

Increased destruction (Felty's syndrome - variant of rheumatoid arthritis involving immune mediated destructio of neutrophils via anti-neutrophil antibodies)
What is leukocytosis?
High number of white blood cells
What is Neutrocytosis?
Neutrophilia

High number of neutrophils

Acute inflammation
Acute infection (especially bacterial)
Certain cancers
Leukemia of neutrophils
What is Eosinocytosis
Eosinophilia

High number of eosinophils

Type I hypersensitivity
Helminthic infections
What is Lymphocytosis?
High number of lymphocytes

Granulomatous diseases
Viral infection
Pertussis (toxin prevents lymphocyte entry to lymph nodes, so increased number in blood)
What is monocytosis?
High number of monocytes

Granulomatous diseases
Infectious mononucleosis
Explain the difference between leukemia and lymphoma
Leukemia: neoplastic WBCs in the blood

Lymphoma: solid tumor of neoplastic lymphocytes
Explain what "Acute" and "Chronic" mean in leukemia
Acute = immature cells

Chronic = mature cells
Acute Lymphocytic Leukemia (ALL)
Overabundance of immature lymphoblasts

Most common malignancy of children

Lymphadenopathy
Impaired bone marrow function
Acute Myelogenous Leukemia (AML)
Overabundance of immature WBCs (other than lymphoblasts)

All ages, but peaks between 15-39

Impaired bone marrow function

Auer rods in myeloblasts (red staining peroxidase positive meedle like structures - evidence of myeloid proliferation)
Chronic Myelogenous Leukemia (CML)
Overabundance of mature WBCs other than lymphocytes

25-60 years old, peak between 30-40
Insidious onset

Impaired bone marrow function

Philadelphia chromosome (9:22 chromosomal translocation to create bcr-abl fusion oncogene)

Low LAP (leukocyte alkaline phosphatase)
Chronic Lymphocytic Leukemia (CLL)
Overabundance of mature lymphocytes

Over 50 years, males > females

Lymphadenopathy
Impaired bone marrow function

Variant: Sezary Syndrome (leukemic portion of mycosis fungoides)
Hairy Cell Leukemia
Mostly in middle aged white men

Rarely hepatomegaly
Splenomegaly (#1 sign)

Involves only B cells
Develop hair-like projections

Impaired bone marrow function

Positive TRAP (tartrate-R-acid phosphatase
CD25 markers present
Hodgkin's Disease
Leukocytosis of PMNs
Reed-Sternberg cells (high number = worse prognosis)
Contiguous spread
Nodal involvement

4 subtypes:
Lymphocyte predominance (best prognosis)
Nodular sclerosis (more common in women, better prognosis than mixed)
Mixed cellularity
Lymphocyte depletion (worst prognosis)
Non-Hodgkin's Lymphoma
Widespread adenopathy
Hypercalcemia
Hepatosplenomegaly
Probably of viral etiology
Associated with bcl-2
Spreads to multiple different nodes
Neutrocytosis