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183 Cards in this Set

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MOA:

Beta Blockers
Decrease activation of beta-1 receptors on heart to decrease cardiac output
This decreases BP and work load of heart

Can help minimize effects of hyperthyroidism (but not treat it)

Decrease renin production due to beta-1 receptors on JG cells
Decreases angiotensin, decreases peripheral resistance to decrease BP
Also decreases sodium and water retention
What are the beta blockers?
-olol

Beta-1 selective:
Atenolol
Nebivolol
Metoprolol

Non-selective, also block alpha-1:
Labetalol
Carvedilol

Non-selective:
Propranolol
Timolol
Pindolol
Nadolol
What are the uses of beta blockers?
Reduce BP (antihypertensive)
Reduce work load of heart to prevent further damage
Reduce sodium and water retention
Maintenance therapy in CHF
Minimize symptoms of hyperthyroidism
Thiazides
Diuretics
Antihypertensive

Block sodium uptake in DCT - increase sodium and water excretion
Decreases blood volume, decreases cardiac output

Adverse effects:
Hypokalemia
Hypercalcemia
Hyperuricemia

Most used: hydrochlorothiazide
Adverse Effects:

Beta Blockers
Fatigue
Insomnia
Impotence
Decreased HDL
Increased triglycerides

Non-selective: may exacerbate COPD or asthma (contraindicated)
Calcium Channel Blockers
Antihypertensive

Block ability of calcium to enter the cell
Calcium plays role in contraction, thus decreasing contraction force
Results in vasodilation and decreased cardiac output with decrease in BP

Diltiazem - affects both vasculature and heart, with more effect on heart
Verapamil - affects both heart and vasculature
Nifedipine - affects vasculature only

Adverse effects:
Constipation
Vertigo
Headache
Fatigue
Hypotension
ACE Inhibitors
Antihypertensive

Blocks conversion of angiotensin I to II
Increases vasodilation, decreases water and sodium retention
Increases bradykinin activity - vasodilation

-pril
Captopril
Lisinopril
Enalapril

Adverse effects:
Dry cough (due to bradykinins)
Rash
Fever
Altered taste
Hypotension
Hyperkalemia
Angioedema
First dose syncope
Fetotoxic
Alpha-Blockers
Antihypertensive

Block alpha receptors to cause arteriolar vasodilation
Reduces peripheral resistance to decrease BP in arteries

Prazosin
Terazosin

Adverse effects:
Reflex tachycardia
First dose syncope
Angiotensin II Antagonists
(Angiotensin Receptor Blockers - ARBs)
Antihypertensive

Block angiotensin II receptor to produce vasodilatoin and decreased aldosterone production
Decreases sodium and water retention, decreases BP

Do not block degradation of bradykinins - not as powerful as ACE inhibitors but eliminates dry cough side effect

-sartan
Losartan
Candesartan
Valsartan
Clonidine
Antihypertensive
Central alpha-2 agonist

Depresses sympathetic outflow, decreases BP by decreasing CNS sympathetic effects on CV system
Hydralazine
Antihypertensive
Smooth muscle relaxant

Decreases BP by causing vasodilation
Alpha-Methyldopa
Antihypertensive
Central alpha-2 agonist

Depresses sympathetic outflow, decreases BP by decreasing sympathetic CNS effects on CV system
Sodium Nitroprusside
Antihypertensive
Vasodilator

Poisonous if given orally - hydrolysis to cyanide
Given IV - rapid and powerful vasodilation of both arteries and veins

Treat adverse effects with sodium thisulfate - binds cyanide to produce less toxic product that can be excreted by kidneys
Minoxidil
Antihypertensive
Vasodilator

Adverse effect: hypertrichosis (excessive hair growth)
What is the first line therapy for all patients to prevent or treat hypertension?
Lifestyle modification

Maintain optimal weight and healthy diet (DASH)
Cessation of smoking
Exercise
Restriction of sodium
Moderation of alcohol consumption
What is the target blood pressure for all patients?
<140/90

If high risk for CAD: <130/80

If history of angina or MI: <130/80

If CHF: <120/80
What is the first line treatment for hypertension?
Thiazides

If stage 2 (>160/100), thiazide plus ACE/ARB or CCB

If chronic renal disease or diabetes: ACE/ARB
What is the treatment for hypertensive patients with history of angina or MI?
Target <130/80

Beta blocker + ACE/ARB

If two agent regimen is not successful, add CCB or thiazide
What is the treatment for hypertensive patients with CHF?
When stable:
Beta blocker + ACE/ARB + diuretic (loop or thiazide)
If severe, + aldosterone antagonist

Verapamil, diltiazem, clonidine, alpha blockers contraindicated

African Americans: + hydralazine or isosorbide dinitrate

Acute exacerbation: stop beta blocker until cardiac output is restored, treat with digoxin
What is a hypertensive emergency?
>210/150 (130 if preexisting condition)

BP must be lowered quickly to avoid end organ damage

TX: sodium nitroprusside (IV), diazoxide, or labetalol
Which beta blocker can prevent reflex tachycardia?
Labetalol - both alpha and beta blocker
Spironolactone
Aldosterone antagonist
Prevents sodium and water uptake - lowers BP

Potassium sparing - works at DCT where potassium is normally exchanged for sodium

Adverse effects:
Hyperkalemia
Metabolic acidosis
Hormone-related side effects (due to structural similarity to sex hormones)
Ergot Alkaloids
Vasoconstrictive - treat migraines

Ergotamine:
5-HT2 (serotonin) antagonist
Used in prodromal period (prevention)
Contraindicated in pregnancy, PVD, CAD

Methysergide:
Used for prevention - prophylactic, not used for active attack
Triptans
Vasodilator - used to treat migraines
Generally more powerful than ergot alkaloids
Can be used for prevention or treatment of acute attack

Cannot be used with Prinzmetal's angina, PVD, uncontrolled hypertension
Should not be used with SSRIs, SNRIs, or MAOIs - could cause serotonin syndrome
Cyproheptadine
Used for prevention of migraine or cluster headache (more common use)
Triptans generally considered superior

5-HT2 receptor blocker
Ondansetron
Granisetron
Dolasetron
Palonosetron
5-HT3 antagonists
Powerful anti-emetic agents
Metoclopramide
5-HT4 agonist
Anti-emetic - causes increased GI motility
Buspirone
5-HT1 agonist
Antianxiolytic
Holoenzyme
Prokaryotic

Core enzyme plus sigma-factor
Sigma Factors
Prokaryotic

Bind to RNA polymerase
Depending on factor, RNA polymerase recognizes certain promoters but not others
Cistron
Prokaryotic

Region of DNA that encodes a single protein
Polymerase I
(Eukaryotic)
Makes rRNA
Polymerase II
(Eukaryotic)
Makes mRNA
Polymerase III
(Eukaryotic)
Makes tRNA
What steps of eukaryotic mRNA are processed in the nucleus?
Addition of 5'-cap of methylated GTP
Poly A tail added to 3' end
Introns removed and exons spliced together
What does "semiconservative" mean in DNA replication?
Parent strands separate and each serves as a template for a newly synthesized one

Replication of eukaryotic DNA is semiconservative
In which direction is DNA read during replication? In which direction is the new strand produced?
Read: 3' to 5'

Produced: 5' to 3'
Helicase
Prokaryotic

Separates parental DNA strands
Primase
Prokaryotic

RNA polymerase that copies parental strand and makes RNA primer
Polymerase III
(Prokaryotic)
Major DNA polymeras in prokaryotes
Replicates both parental strands
Has proofreading ability
Has 3' exonuclease activity to remove wrong nucleoties
Polymerase I
(Prokaryotic)
Removes primer and fills gap with DNA
5' exonuclease activity
Polymerase II
(Prokaryotic)
DNA repair
3' exonuclease activity
Ligase
Prokaryotic and eukaryotic

Joins Okazaki fragments of lagging strand
DNA Replication:

Delta
Eukaryotic

Major DNA polymerase
Produces leading strand
Has helicase activity
No proofreading
No exonuclease activity
DNA Replication:

Alpha
Eukaryotic

DNA polymerase
Produces lagging strand
Has primase activity
DNA Replication:

Beta, Epsilon
Eukaryotic

Minor DNA polymerase
DNA repair
3' exonuclease activity
DNA Replication:

Gamma
Eukaryotic

Mitochondrial DNA polymerase
Endonuclease
Incision of DNA
Exonuclease
Removal of nucleotides from incised end
Which malignancies develop in organs derived from each germ layer?
Ectoderm and endoderm: adenomas and carcinomas

Mesoderm: sarcomas and fibromas
Ectoderm
Neural tube -> CNS
Neural crest -> PNS
Placodes -> sensory organs
Surface epithelium -> skin
Mesoderm
Somites -> muscles, vertebral column

Connective tissue
Lymphatic tissues
Blood cells
Endoderm
Epithelium of GI tract
Liver
Pancreas
Thymus
Thyroid
What vessels are contained in the umbilical cord?
2 arteries (carrying deoxygenated blood)
1 vein (carrying oxygenated blood from placenta)
What is connected by the yolk stalk?
Yolk sac to GI tract
What is connected by the urachus?
Urinary bladder to allantois
Remnants:

Umbilical Arteries
Medial umbilical ligaments
Remnants:

Urachus
Median umbilical ligament
Remnants:

Umbilical Vein
Round ligament
Remnants:

Ductus Venosus
Venous ligament
Remnants:

Ductus Arteriosus
Ligamentum arteriosum
Remnants:

Yolk Stalk
Meckel's diverticulum

Rule of 2s:
2% of people
Located within 2 feet of ileocecal junction (at antimesenteric border of ileum)
About 2 cm long

Inflammation may mimic appendicitis
Derivates of Branchial Arch 1
(Mandibular Arch, Meckel)
Bones: malleus, incus

Muscles: muscles of mastication

Arteries: facial artery

Nerves: V3
Derivates of Branchial Arch 2
(Hyoid Arch, Reichert)
Bones: stapes, styloid, lesser horn of hyoid

Muscles: muscles of facial expression

Arteries: external carotid artery

Nerves: VII
Derivates of Branchial Arch 3
(Thyrohyoid Arch)
Bones: body of hyoid

Muscles: stylopharyngeal muscles

Arteries: internal carotid artery

Nerves: IX
Derivates of Branchial Arch 4
Bones: larynx

Muscles: pharyngeal muscles

Nerves: X
Tissues Derived from Pharyngeal Pouch 1
Tympanic cavity
Eustachian tube
What is formed from the first pharyngeal cleft?
Forms external auditory meatus

Only cleft that does not disappear
Tissues Derived from Pharyngeal Pouch 2
Palatine tonsils
Tissues Derived from Pharyngeal Pouch 3
Ventral: thymus
Dorsal: inferior parathyroids
Tissues Derived from Pharyngeal Pouch 4
Ventral: nothing
Dorsal: superior parathyroids
Tissues Derived from Pharyngeal Pouch 5
Ultimobranchial body -> parafollicular C cells of thyroid
What are cervical cysts?
Remnants of pharyngeal clefts
Uncommon

Located in anterolateral part of neck
1-2 inches in diameter
Urogenital Development
7th week

Male:
Wolffian (mesonephric) ducts become epididymis and vas deferens
Mullerian (paramesonephric) ducts disappear
Wolffian (mesonephric) sustained by testosterone from Leydig cells
Mullerian (paramesonephric) suppressed by MIF glycoprotein from Sertoli cells

Female:
Wolffian ducts disappear
Mullerian ducts become fallopian tubes, uterus, vagina (down to hymen)

Both:
Allantois becomes urinary bladder and urachus
Ureteric bud (inferior part of mesonephric duct, metanephric) becomes bladder trigonum, ureter, collecting tubule
Pronephros and mesonephros diseappear (pro never functional, meso only temporarily)
Metanephros becomes kidneys
What Passes Through:

Optic Canal
Optic nerve
Ophthalmic artery
What Passes Through:

Superior Orbital Fissure
Cranial nerves III, IV, V, VI
Sympathetic nerves
Ophthalmic veins
What Passes Through:

Foramen Rotundum
Cranial nerve V (maxillary branch)
What Passes Through:

Foramen Ovale
Cranial nerve V (mandibular branch)
Accessory meningeal artery
What Passes Through:

Foramen Spinosum
Middle meningeal artery
What Passes Through:

Foramen Magnum
Spinal cord
Accessory nerve
Vertebral arteries
Spinal arteries
What Passes Through:

Jugular Foramen
Cranial nerves IX, X, XI
Internal jugular vein
What Passes Through:

Hypoglossal Canal
Cranial nerve XII
What Passes Through:

Internal Auditory Meatus
Cranial nerves VII, VIII
Labyrinthine artery
What is a sign of a basilar skull fracture?
Bruising over mastoid process or periorbital region
Eye Muscle:

Medial Rectus
Moves eye nasally

Innervation: III
Eye Muscle:

Lateral Rectus
Moves eye temporally

Innervation: VI
Eye Muscle:

Superior Rectus
Moves eye up and nasally
Rotates medially
Combines with inferior oblique to raise eye upward

Innervation: III
Eye Muscle:

Inferior Oblique
Moves eye up and temporally
Rotates laterally
Combines with superior rectus to raise eye upward

Innervation: III
Eye Muscle:

Inferior Rectus
Moves eye down and nasally
Rotates laterally
Combines with superior oblique to move eye downward

Innervation: III
Eye Muscle:

Superior Oblique
Moves eye down and temporally
Rotates medially
Combines with inferior rectus to move eye downward

Innervation: IV
Abducens Paralysis
Unable to abduct eye on affected side
Diplopia (double vision)
Trochlear Paralysis
Slight vertical double image
Patient compensates by tilting head
Dilator Pupillae
Internal eye muscle

Function: mydriasis (dilation of pupil)

Innervation: sympathetic
Sphincter Pupillae
Internal eye muscle

Function: miosis (constriction of pupil)

Innervation: parasympathetic
Ciliary Muscle
Internal eye muscle

Function: accommodation (contraction of muscle relaxes ligaments to allow lens to become round for near vision)

Innervation: parasympathetic
Levator Palpebrae Superior
Eyelid muscle

Function: raises lid

Innervation: III
Muller's Muscle
Eyelid muscle

Function: raises lid

Innervation: sympathetic
What happens to the eyelid muscles in drowsiness?
Reduced sympathetic tone
Muller's muscles relax
Eyelid droops
Horner's Syndrome
Caused by neck injuries or tumors interrupting cervical sympathetic chain

Miosis
Ptosis
Red and dry facial skin on affected side (cannot sweat)
What are the muscles of the tongue and their functions?
Genioglossus - pulls tongue out

Styloglossus - pulls tongue in and up

Hyoglossus - pulls tongue down
What is caused by damage to the hypoglossal nerve (CN XII)?
Genioglossus muscle of healthy side becomes dominant
Tongue will deviate toward side of damage
What is the sensory innervation of the tongue?
Anterior 2/3: taste - VII, touch/temp - V3

Posterior 1/3: taste - IX, touch/temp - IX
What are the muscles of the mandible and their functions?
Lateral pterygoid, digastric, geniohyoid - open mouth

Masseter, medial pterygoid, temporalis - close mouth

Lateral pterygoid - protrudes mandible, lateral displacement

Temporalis - retracts mandible
What may be fractured by a blow to the jaw?
Neck of mandible
Region of opposite canine tooth
What are the muscles of the larynx, their functions, and their innervations?
Posterior cricoarytenoid - opens glottis - recurrent nerve

Lateral cricoarytenoid - closes glottis - recurrent nerve

Thyroarytenoid - relaxes vocal cords - recurrent nerve

Cricothyroid - tightens vocal cords - superior laryngeal nerve
What happens with damage to the recurrent nerves of the neck?
Unilateral damage - hoarseness
Bilateral damage - dyspnea

Left wraps around aortic arch
Right wraps around right subclavian artery

High risk procedures: thyroidectomy, carotid endarterectomy, operations in anterior triangle of neck
What nerves are responsible for the sensation of the larynx?
Above glottis - superior laryngeal nerve
Below glottis - recurrent nerve

Important to initiate cough reflex
What are the muscles of the shoulder, their functions, and their innervations?
Pectoralis major - adduction - C5-T1

Deltoid and serratus anterior - abduction (first 60 deltoid, then serratus) - long thoracic nerve

Deltoid - anteversion - axillary nerve

Teres major - retroversion - subscapular nerve

Infraspinatus - external rotation - suprascapular nerve

Subscapularis - internal rotation - subscapular nerve
Scapular Winging
Medial border of scapula stands out when person presses arm anteriorly against a wall

Causes:
Paralysis of anterior serratus muscle
Damage to long thoracic nerve
Rotator Cuff
Supraspinatus
Infraspinatus
Teres minor
Subscapularis

Hold head of humerus in glenoid cavity
Injury causes instability of shoulder joint
What exacerbates pain with inflammation of subacromial bursa?
Abduction
Brachial Plexus
(Basic Details)
Rami C5-C6 - upper trunk - musculocutaneous nerve

Ramus C7 - middle trunk - axillary nerve and radial nerve (posterior cord) and median nerve

Rami C8-T1 - lower trunk - ulnar nerve
Upper Brachial Plexus Injury
Forceful separation of neck and shoulder (motorcycle accidents, football tackling)

Arm hangs in medial rotation ("waiter's tip position")
Posterior Cord Injury
Radial nerve injury
Compression by too long crutches

"Wrist drop"
Lower Brachial Plexus Injury
Forceful pull of arm/shoulders (such as in birth)

Ulnar nerve injury
"Claw hand"
Radial Nerve Injury
"Wrist drop"
Loss of triceps reflex
Sensory loss to posterior arm and dorsal hand
Median Nerve Injury
No flexion of thumb, index and middle fingers
No thumb opposition
Thenar atrophy
Sensory loss to radial 2 1/2 fingers (palm and tips)
Ulnar Nerve Injury
"Claw hand"
No flexion of 4th and 5th fingers
Apothenar atrophy
Sensory loss to ulnar 1 1/2 fingers (palm and tips)
Musculocutaneous Nerve Injury
No elbow flexion
No supination
Loss of biceps reflex
Sensory loss to extensor aspect of forearm
Carpal Tunnel Syndrome
Compression of median nerve by carpal ligament

Pain/tingling in distribution area of median nerve
What nerve is most at risk of injury from a humerus fracture?
Radial nerve (spirals down near humerus)
What is a Colles' fracture?
Fracture of radius near wrist

Dorsal/lateral position of hand
Tennis Elbow
Repetitive stress, especially backhand play
Due to inflammation of lateral epicondyle (origin of extensor muscles of forearm)
Elbow joint and olecranon not involved
What are the muscles of the elbow, their functions, and their innervations?
Biceps brachii - flexion, supination - musculocutaneous nerve

Triceps brachii - extension - radial nerve

Pronator teres - pronation - median nerve
What are the muscles of the hip, their functions, and their innervations?
Gluteus maximus - external rotation, extension - inferior gluteal nerve

Gluteus medius and minimus - internal rotation - superior gluteal nerve

Iliopsoas - flexion - femoral nerve

Gluteus medius - abduction - superior gluteal nerve

Adductor magnus and minimus - adduction - obturator nerve
What is the major risk in pelvic fractures?
Risk of severe internal bleeding

Cause: car accidents
What is the major risk in femoral neck fractures?
Risk of femur head necrosis
Significant morbidity and mortality

Common in elderly women with osteoporosis
What is jaundice?
Also called icterus

Yellowish pigmentation of skin, tissues, and certain body fluids due to deposition of bilirubin pigments
What is the first evidence of jaundice?
Scleral icterus

>5mg/dL, sublingual icterus can be seen (indication of elevated bilirubin due to biliary or hepatic causes)
What are the steps in bilirubin formation?
RBCs die or lyse and release hemoglobin
Heme
(heme oxygenase)
Biliverdin
(biliverdin reductase)
Unconjugated bilirubin
Binds to albumin to be delivered to liver via serum
Conjugated in liver by uridine diphosphate glucuronosyl transferase
Conjugated bilirubin released to intrahepatic bile ducts
What are the primary causes of jaundice?
Hemolysis (elevated unconjugated/indirect)
(G6PD deficiency, sickle cell, autoimmune hemolytic anemia)

Deficiency of glucuronosyl transferase (elevated unconjugated/indirect)
(Gilbert's syndrome, Crigler-Najjar)

Defects in transport of bilirubin from hepatocyte to bile duct (elevated conjugated/direct)
(viral hepatitis, infectious mononucleosis, Rotor syndrome, Dubin-Johnson syndrome)

Obstruction of biliary system (elevated conjugated/direct)
(choledocholithiasis, sclerosing cholangitis, primary biliary cirrhosis)
Gilbert Syndrome
Congenital cause of jaundice

Mildly decreased expression of uridine diphosphate glucuronosyl transferase
Causes elevated indirect bilirubin at times of physical stress
Crigler-Najjar Syndrome
Congenital cause of jaundice

Type 1:
Autosomal recessive
Absent UGT expression (no conjugation occurs)
Lethal

Type 2:
Autosomal dominant
Decreased expression of uridine diphosphate glucuronosyl transferase
Chronic elevation of indirect/unconjugated bilirubin
Rotor Syndrome
Congenital cause of jaundice

Impaired hepatocellular secretion secondary to carrier defect
Causes elevated direct/conjugated bilirubin
Dubin-Johnson Syndrome
Congenital cause of jaundice

Impaired hepatocellular secretion secondary to carrier defect
Darkly pigmented liver
Elevated direct/conjugated bilirubin
Hepatitis A
Only acute, never chronic (no carriers)
RNA virus (picornavirus)
Fecal/oral transmission via contaminated food and water

Acute: HAV IgM
Late: HAV IgG - can last for years, protective

Incubation: 2-6 weeks
Hepatitis B
"Serum hepatitis"
DNA virus (hepadnavirus)

HBs-Ag is earliest marker - indicates current or chronic infection
HBe-Ag indicates highly infective state
10% become chronic

Parenteral, sexual, vertical transmission

Incubation: 2-6 months
What is a Dane Particle?
Hepatitis B viral particle
Hepatitis C
Leading infectious liver disease of Western world
Most important cause of transfusion hepatitis (90%)

RNA virus (flavivirus)

Causes episodic increases in transaminases (ALT, AST) with normal intervals

Parenteral transmission
50-70% become chronic

Incubation: 1-2 months
Hepatitis D
Delta virus
RNA virus
Occurs only in conjuction with HBV - requires HBV's antigen coat for replication

2 types:
Coinfection - HBV and HDV acquired simultaneously
Superinfection - HBV established before HDV acquired (significantly increases mortality associated with HBV)

Parenteral and sexual transmission
Hepatitis E
Self-limited - never chronic (but often fulminant in pregnant women)
Occurs primarily in SE Asia and middle East

Fecal/oral transmission via contaminated water
Hepatitis G
Exact role in acute or chronic disease is not yet understood
Caused by GB virus-C (GBV-C) - RNA virus (Flaviviridae family)
What are some non-infectious etiologies of acute hepatitis?
Drugs
Poison mushrooms
What are some non-infectious etiologies of chronic hepatitis?
Wilson's disease
Alpha-1-antitrypsin deficiency
Chronic alcoholism
Drugs
Autoimmune disease
HBs-Ag
Surface antigen of hepatitis B
Indicates current infection

Appears weeks prior to symptom onset
Persists 3-4 months (if >6 months, indicates carrier state/chronic HBV)
Anti-HBc
Antibody to core of hepatitis B virus
Indicates exposure (past or present infection)

Appears 4 weeks after HBs-Ag appearance
Remains elevated for years after infection
Present during the "window" period
Is not protective
HBe-Ag
Appears after HBs-Ag appears, disappears before HBs-Ag disappears
Secreted by actively infecting virus

Indicates state of extreme infectiousness
HBV DNA
Present in serum of those with current infection
Used to determine viral load after diagnosis
Higher value = more infectious
Present during "window period"
Anti-HBs
Antibody to hepatitis B surface antigen

Appears after symptoms disappear
Indicates immunity - is protective
Toxic Hepatitis
Inflammation of the liver (hepatitis) due to toxin (poison or drug)

Can develop over weeks to months
Looks the same as chronic viral hepatitis histologically

Major causes:
Methotrexate
Chloramphenicol
Halothane
Isoniazid
Cirrhosis
Diffuse disorganization of normal hepatic structure by regenerative nodules surrounded by fibrotic tissue

End stage of many liver diseases
One of top causes of death of 45-65 year olds in USA
Symptoms of Cirrhosis
Weakness
Malaise
Weight loss
Anorexia
Fat malabsorption
Bleeding problems
Ascites
Caput medusa
Infections
Fat soluble vitamin deficiencies
Hepatic encephalopathy
Portal hypertension with varices
Alcoholic Cirrhosis
(Laennec's Cirrhosis)
Irreversible
Most common cause of cirrhosis
End stage of alcoholic hepatitis

Initiated by alcoholic hepatitis, which progresses to fatty change, focal necrosis, neutrophil infiltrates, presence of Mallory bodies

Continued inflammation leads to cirrhosis by causing hepatocyte destruction and scar formation
Liver becomes increasingly fibrotic, leading to central vein obstruction and fibrosis surrounding individual liver cells

Early stage: micronodular
Late stage: macronodular
Cirrhosis due to Viruses or Toxins
Typically initiated by toxic or infectious hepatitis

Common etiologic agents:
Methotrexate
Amiodarone
Hepatitis B
Hepatitis C
Primary Biliary Cirrhosis
No symptoms in early stage
First sign is increased alkaline phosphatase
First symptom is pruritis, especially at night

Peak age: 40-60 years
Female >>>> Male
Micronodular

Autoimmune disease with anti-mitochondrial antibodies
Hemochromatosis
"Bronze diabetes"

Male > Female symptomologically in early years (menses is "protective" from effects)
Autosomal recessive

Increased iron absorption leads to iron deposits in liver, heart, pancreas, and skin in form of hemosiderin

Triad:
Cirrhosis
New-onset diabetes
Skin pigmentation
(Cardiomyopathy is also a frequent outcome)
Wilson's Disease
Also called hepatolenticular degeneration
Autosomal recessive

Accumulation of copper, which may lead to fulminant hepatitis and later cirrhosis

Marked by decreased serum ceruloplasmin so copper deposits inappropriately in:
Brain (psychosis, athetosis, incoordination)
Kidney (high urinary copper)
Cornea (Kayser-Fleischer rings - orange rings visible in cornea)
Liver (cirrhosis)
Amyloidosis
Disease marked by accumulation of amyloid
Affects liver 50% of the time
Metastatic Liver Cancer
Most common type

Primary sites: breast, lung, colon
Hepatocellular Carcinoma
Primary liver cancer
Associated with massive hepatomegaly at tumor site
Massively elevated alkaline phosphatase, modest elevations in ALT and AST
Tumor marker: alpha fetoprotein

Most common causes: chronic HBV or HCV, aflatoxin exposure
Cholangiocarcinoma
Bile duct carcinoma
Greatest risk factor: infection with liver fluke (Clonorchis sinensis)
Starts in intrahepatic bile ducts
More common in Asia
Pancreatitis
Major causes: alcoholism, gallstones (obstructing pancreatic duct system), hypertriglyceridemia

Severe epigastric pain with radiation to back
Elevated amylase and lipase
Hypercalcemia can occur (calcium binding to fats being digested by pancres)
Inappropriate activation of pancreatic enzymes leading to autodigestion of pancreas - can be life threatening
Intussusception
One part of bowel telescopes into neighboring bowel
Usually involves terminal ileum intussuscepting into ascending colon

Risk age: up to 7 years old, highest risk is 5-10 months old
Most significant risk: adenovirus infection

Symptoms:
Vomiting
Palpable right upper quadrant sausage-shaped mass with vacant lower right quadrant
Currant jelly stool
Midgut Volvulus
Duodenum and colon malrotate around mesentery during fetal development, causing constriction of bowel and vasculature

Age: neonates (under 30 days old)

Symptoms:
Vomiting
Bloody diarrhea
Abdominal distention
Necrotizing Enterocolitis
Bowel mucosa necroses, eventually deeper bowel tissues

Age: neonates
Risks: maternal NSAID use, prematuturity, comorbid disease at birth
Hirschprung's Disease
Due to lack development of Auerbach's and Meissner's plexuses in focal regions of colon
No peristalsis occurs in affected areas

Age: neonates

Symptoms:
Vomiting
Obstipation
Chronic abdominal pain
Osteoarthritis
#1 articular disorder
Disorder of hyaline cartilage and subchondral bone - all surrounding tissues hypertrophied
Cartilage is lost, joint spaces narrow, subchondral bone increases in density, osteophytes form
Slow, progressive

Etiology: use, trauma
Starts in teens-20s (asymptomatic), most people have it by age 40 (usually still asymptomatic), universal in population by age 70
Female > Male (symptomologically)

Joint stiffness after inactivity
Stiffness lasts less than 1 hour after waking
Knees, hips, spine (weight bearing joints) most affected - DIPs of hand and great toe also affected
Heberden's nodes and Bouchard's nodes (palpable osteophytes at interphalangeal joints)
No serologic marker
Eburnation (polished appearance of bone due to wearing)
Joint mice common (bits of bone in joint space from osteophyte fractures)
Rheumatoid Arthritis
Must have 4 of 7 criteria for diagnosis
Characterized by non-specific, usually symmetric inflammation of peripheral joints
Abrupt onset with multiple joint involvement
Synovial membrane proliferation (pannus formation) with erosions of cartilage and subchondral bone, also soft tissue swelling

Etiology: autoimmune
Primarily females, 20-50 years at onset

Tenderness in all active (inflamed) joints
Stiffness lasts more than 1 hour after waking
Starts in small joints, especially PIP and MCP
Rheumatoid nodules (palpable subcutaneous soft tissue nodules on extensor surfaces, particularly of hands and arms)
Increased ESR or CRP, Rheumatoid factor, HLA-DR4/Dw4/Dw14
Erosions in bone secondary to destruction via membrane attack complex
7 Criteria for Rheumatoid Arthritis
Need 4 for diagnosis

Morning stiffness > 1 hour
Arthritis in 3 or more joints simultaneously
Arthritis in hand joints
Symmetrical arthritis
Rheumatoid nodules
Serum rheumatoid factor
Erosions or bony decalcification identifiable on Xray
Still's Disease
Systemic juvenile arthritis, juvenile rheumatoid arthritis

Acutely febrile
Polyarthritis
Rheumatoid factor negative
Micrognathia
Occurs before age 16, complete remission by adulthood
Psoriatic Arthritis
Like rheumatoid arthritis but also associated with psoriasis of skin and/or nails

No rheumatoid factor
Affects primarily DIPs
Sausage digits
HLA-B27
Felty's Syndrome
Polyarticular rheumatoid arthritis
Splenomegaly
Leukopenia (specifically with neutropenia)
Leg ulcers
Increased infections

Severe variant of RA
Osteogenesis Imperfecta
Abnormal fragility of bone due to disorder of collagen synthesis

Increased number of fractures
Blue sclera (thin connective tissue reveals underlying vessels)

Newborn type is most severe (skull feels like "bag of bones" - soft with Wormian bones)
Osteopetrosis
Also called Marble Bones or Albers-Schonberg Disease

Sclerosis of vertebral endplate ("rugger jersey" vertebrae on Xray)
Increased density and abnormal skeletal modeling
Very brittle bones

Many forms - can be fatal (though most are not)
Achondroplasia
Type of chondrodystrophy - defective cartilage synthesis and decreased epiphysis formation

Type of dwarfism
Autosomal dominant
Short limbs with normal sized head and trunk
Aseptic Necrosis
Due to cut in blood supply
Can be secondary to trauma at head of femur, tibial tuberosity, scaphoid bone

Osgood-Schlatter disease - aseptic necrosis of tibial tuberosity
Legg-Calve-Perthes Disease - aseptic necrosis of femoral head in children without trauma history
Osteoporosis
Thinned cortical bone and enlarged medullary cavity
Diffuse radiolucency
No serum markers or abnormalities - test with bone density or DEXA scan

Fragile bones that are inadequate for weight bearing or mild trauma
Patients easily fracture bones with falls, suffer commonly from compression fractures of vertebrae (from weight bearing)

Risk groups: Caucasians, women, petite individuals
Etiologies of Osteoporosis
Estrogen deficient state:
Post-menopausal, post-overiectomy, ovarian failure

Physical inactivity:
Being bedridden

Hypercortisolism:
Cushing's, chronic steroid therapy

Hyperthyroidism

Subclinical calcium deficiency
Types of Osteoporosis
Primary:
Idiopathic - children and adolescents
Type I - postmenopausal women
Type II - men and women over 70

Secondary:
All other causes
Osteomalacia
Due to inadequate bone mineralization
In children known as rickets when caused by vitamin D deficiency

Serum findings: low calcium, low phosphate, high alkaline phosphatase
Radiologic findings: diffuse radiolucency with occasional "Looser's Zones" (radiolucent bands that run perpendicular to periosteal surface, due to pseudofractures)

Results in bone pain, skeletal deformities (especially long bone bowing), frequent fractures
Etiologies of Osteomalacia
Vitamin D deficiency

Severe liver disease of any type:
Liver is needed to convert Vitamin D3 (second to last step in making active vitamin D)

Anticonvulsant drugs

Renal osteodystrophy:
Kidney completes last step of creating active vitamin D

Fanconi's Syndrome (disorder affecting renal tubules, causing loss of phosphate and calcium)

Malnutrition/Malabsorption:
Anything that limits availability of calcium, phosphate, vitamin D
Osteitis Fibrosa Cystica
Von Recklinghausen disease of bone

Focal bony damage caused by severe hyperparathyroidism
Results from microfractures and secondary hemorrhages that cause ingrowth of fibrous tissue along with hemosiderin deposition
"Tumors" often undergo cystic degeneration
Paget's Disease
Osteitis deformans

Increased uncontrolled bone turnover with formation outpacing resorption and formation being of disorganized bone

Results in frontal bossing, deafness, bone pain, pain secondary to compression fractures, chalkstick fractures of lower extremities, high output cardiac failure

Lab findings: extremely high alkaline phosphatase, possible occasional hypercalcemia (at times of "remission" of bony overgrowth)
Radiologic findings: enlarged thickened bones with coarse thickened cortices