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281 Cards in this Set

  • Front
  • Back
Blood
a liquid tissue containing seven types of cells that are suspended in a watery substance called plasma
Types of white blood cells (leukocytes)
basophils, eosinophils, neutrophils, lymphocytes, monocytes (become macrophages)
Functions of Blood (3)
1. Transport oxygen and carbon dioxide
2. Transport of ions, glucose, wastes, and hormones
3. Acts as a defense for the body against foreign materials.
Where are blood cells produced?
Bone Marrow
What single type of cell does blood form from?
Multipotent Stem Cell
Erythropoietin (EPO)
produced by kidneys and increases production of red blood cells (tells bone marrow to produce more RBCs)
Thrombopoietin (TPO)
increases production of platelets
Interleukin-7
major cytokine that stimulates stem cells to increase lymphocytes
Anemia
shortage of RBCs, shortage of amount of hemoglobin in them, most commonly caused by inadequate intake of iron
Definition of Anemic and tx
hemoglobin < 10.....treat with PROCRIT
#1 WBC
T Lymphocytes
Where do T Cells migrate from the bone marrow to mature?
Thymus
Components of Blood Plasma and Percentages
Water 92%
Proteins 6%
Salt 0.8%
Lipids 0.6%
Glucose 0.2%
Site of occlusion in vein occlusion
lamina cribrosa
How can you tell a vein occlusion is non-ischemic?
LACK of hemes, CWSs, APD, and being able to see underlying choroid, px has good VA
What is the main concern in ischemic CRVO?
neovascular glaucoma
What is a big cause of CRVO?
glaucoma (bc lamina cribrosa is compressed in glaucoma)
Hypoperfusion Retinopathy/Ocular Ischemic Syndrome
usually unilateral, males > females 2:1, *dot/blot hemes and microanuerysms found only in mid-periphery (=Hypoperfusion Retinopathy); when above are associated with neo of disc, retina, iris, or angle = Ocular Ischemic Syndrome
Pathogenesis of OIS
atheromatous ulceration and stenosis at bifurcation of common carotid artery
Symptoms of OIS (know)
1) ocular and periorbital pain in 40% of cases
2) prolonged recovery of vision following exposure to bright light (Light Induced Amaurosis)
3) Amaurosis Fugax (TMB) in 5% of cases
4) TIAs
Ocular Signs in OIS
1) dilated but not tortuous veins
2) retinal hemes in mid-peripheral retina (80%)
3) CWSs (5%)
4) Neo of disc (35%)
5) Neo of retina (8%)
6) rubeosis iridis (65%)
7) uveitis- mild anterior (20%)
What should you think if you see uveitis in older px?
Carotid artery disease
Work up for OIS
Carotid artery evaluation & echocardiogram
Tx for OIS
carotid surgery if needed, aspirin, PRP for neo, stop smoking
1st and 2nd leading causes of death in OIS
1) Ischemic heart disease
2) Stroke
Hypercoaguable State
px is constantly making clots bc factor 5 is always turned on (someone below age 50 should not have vein occlusion; if they do, should think hypercoaguable state)
Primary State conditions that can cause ocular problems (know)
1. Protein C deficiency
2. Protein S deficiency
3. Antithrombin III
4. Factor V Leiden ** (1 out of 10 ppl)
5. Hyperhomocysteinemia
6. Prothrombin 20210 mutation
7. Antiphospholipid syndrome- miscarriages
What proteins turn off the coagulation pathway?
Protein C and S
Protein C or S deficiency/Antithrombin III deficiency
these proteins normally turn factor 5 off; deficiency would leave factor 5 on constantly resulting in venous thromboembolism
What is the most common hereditary blood coagulation disorder in US?
Factor V Leiden
Factor V Leiden
a defect in factor 5 so that it can never be turned off; resistant to Protein C, found in 10% of caucasions, rare in AA and asians
Hyperhomocyteinemia
causes high levels of the amino acid homocysteine; leads to artery and vein occlusion, stroke, upward lens subluxation, heart attack in older males, **treat with B6, B12, and folic acid
Prothrombin 20210 gene mutation
**second most common hereditary blood coagulation disorder; elevated levels of plasma prothrombin; increased risk of venous thrombosis; 4% of Caucasians
Antiphospholipid syndrome
antibodies to phospholipids activate coagulation cascade; **can lead to BOTH artery and vein occlusions; cause of most miscarriages
Tx of Hypercoaguable State
Coumadin, Heparin, Aspirin therapy**
What ocular finding is characteristic of carotid artery disease?
midpeipheral hemes
What do you have to rule out if you see someone younger than 50 with a vein occlusion?
hypercoaguable state
Hyperviscosity Syndromes
if px makes too many RBCs, WBCs, or platelets, buildup occurs and their byproducts make the blood very thck
3 types of Hyperviscosity Syndromes
1. Waldenstrom Macroglobulinemia (IgM)
2. Multiple Myeloma (tumor of B cells)
3. Leukemia
What is the hallmark ocular sign of hyperviscosity?
Sausage Link Vessels
What is a bilateral vein occlusion indicative of?
Hyperviscosity
Tx of Leukemia
Chemo and radiation therapy (ocular manifestations resolve after tx)
Types of Leukemia
1. Chronic Lymphocytic Leukemia
2. Chronic Myeloid Leukemia
3. Acute Lymphocytic Leukemia
4. Acute Myeloid Leukemia **most common
Multiple Myeloma
malignant plasma cell tumor- end stage B lymphocyte; tumors cells produce massive quantities of IgG or IgA
Waldenstrom macroglobulinemia
neoplastic B cells produce IgM at too high of a rate
Anemia
decrease in RBC count, hemoglobin, orhematocrit
Causes of Anemia
1. decreased RBC production
2. hemotopoietic cell damage from infection, drugs, or radiation
3. deficiency of factors like iron necessary for heme synthesis
4. increased RBC loss from external blood loss or red cell destruction
Sickle Cell Retinopathy KNOW
1. Seafan neo
2. Black sunbursts- RPE hyperplasia
3. Salmon Patch Hemorrhages
***7 types of blood cells
1. RBCs (Erythrocytes)
2. Platelets (Thrombocytes)
3. White Blood Cells (Leukocytes)
a. Basophils
b. Eosinophils
c. Neutrophils
d. Lymphocytes
e. Monocytes- become macrophagesd
Difference between hypercoaguable and hyperviscosity
1. Hypercoaguable=blood clots; mid-peripheral hemes
2. Hyperviscosity=too many cells and cell by-products; bilateral vein occlusions
Tx of Hypercoaguable syndromes vs Hyperviscosity syndromes
1. Hypercoaguable- Coumadin, Heparin, Aspirin
2. Hyperviscosity- chemo or radiation therapy, bone marrow transplantation
Most common and second most common coaguable states
1. Factor V Leiden
2. Prothrombin 20210 gene mutation
Normal INR (International Normalized Ration) for a px on Coumadin
2.0-3.0
What disease do 50% of Giant Cell pxs have?
Polymyalgia Rheumatic (PMR)- stiffness in neck, shoulder, and hip
Ocular Manifestions of Giant Cell
#1. ION
2. acute painless vision loss
3. pale swelling of optic nerve head with flame shaped hemes
4. CRAO
5. CN 3, 4, 6***
6. CWSs
7. OIS
8. Cilioretinal Artery Occlusion
9. Must refer to ER for sed rate and C-reactive protein
Etiology of AAION (vs NAION)
occlusion of short posterior ciliary arteries with giant white blood cells
Systemic Presentation of AAION
Headache, scalp tenderness, jaw claudication, night sweats, weight loss, fever, PMR, depression
Systemic Testing for AAION
Immediate C-reactive protein, CBC w/ platelets, Westegren Sed. Rate, carotid artery evaluation, echocardiogram, fluorescein angiography
Tx for AAION
IV steroids, temporal artery biopsy, followed by oral steroid
Blood aqueous barrier
tight junctions between non-pigmented epithelial cells of ciliary body and blood vessels of iris
Most common WBC?
T cell (apprrox 70%)
What produces antibodies
B cells
What matures in bone marrow?
B cells
What matures in thymus?
T cells
What must you rule out if you see hemorrhages in mid-periphery?
carotid artery disease
2 main causes of carotid artery disease?
1. cholesterol buildup due to high cholesterol
2. GCA
Is tehre pain with carotid artery dx?
yes; known as ocular angina from OIS
Most common hypercoaguable syndrome?
Factor V
Tests for GCA?
C-reactive protein and ESR
Are RBCs nucleated?
NO
Which blood type is the universal recipient?
Group AB- cant give blood to anyone unless AB too
Which blood type is the universal donor?
Group O- has neither A or B antigens
Hemoglobin
Oxygen carrying molecule (marrow stimulated to make hemoglobin by EPO; kidneys produce EPO in response to hypoxia)
Microcytic Anemias (MCV<80)
small red blood cells from:
1. iron deficiency**
2. thalassemias
3. sideroblastic anemias
4. lead poisoning
Normocytic Anemias (MCV 80-100)
1. anemia of chronic disease**
2. aplastic anemia
3. sickle cell disease
4. bone marrow infiltration
5. blood loss/hemolysis
Macrocytic Anemias (MCV>100)
1. liver disease
2. myelodysplasia
3. elderly
4. hypothyroidism
5. alcohol
6. drug induced
7. hemolysis
8. megaloblastic anemias (vitamin B12 and folate deficiencies**)
Most common cause of anemia?
iron deficiency (most common) and anemia of chronic disease
Initial Tests to oder in anemia
CBC, reticulocyte count, peripheral smear, iron, folate, and B12 levels
Sideroblastic Anemia
teardrop shaped cells
Megaloblastic Anemia
oval macrocytes, hypersegmented neutrophils, vitamin B121 or folate deficiency
Neutrophils (myeloid family)
mobile phagocytes, kill organisms covered with antibodies, fight bacterial infections, clean up dead/damaged tissue
Basophils (myeloid family)
granules contain histamine and heparin, role in immedate hypersensitivity rxns
Eosinophils (myeloid family)
increased numbers in parasitic infections
Monocytes (myeloid family)
clean up debris, phagocytic
T-cells (lymphoid family)
70%; initiate and regulate immune response; fight viral infections
B-cells (lymphoid family)
synthesize and secrete antibodies
Platelets
1st responder to stop bleeding
Hemophilia- The Prototypical Coagulation Factor Deficiency
X-linked recessive, low factor VIII or IX levels, deep soft tissue bleeds in joints and muscles, NO PETECHIAE**, tx w/ transfusion of deficient factors
2 drugs that deactivate key clotting factors
Heparin and Warfarin
Acquired Hypercoaguable States- Virchow's Triad
1. alteration in blood flow (venous stasis)
2. injury to vascular endothelium- major trauma
3. alteration in constitution of blood (hypercoaguability) from cancer, smoking, birth control pill, etc
Symptoms of Acute Leukemia
1. decrease WBC: fever, infection
2. decrease RBC: fatigue, pallor
3. decrease PLT: bleeding
4. enlarged liver, spleen lymph nodes
*adults: 80% myelogenous (AML), 20% lymphoblastic (ALL)
Autologous (Bone Marrow Transplantation)
stem cells harvested from patient himself
Allogeneic (Bone Marrow Transplantation)
stem cells harvested from a matched donor
What kind of cells are present in Hodgkins (younger pxs) and non-hodgkins (older pxs)?
Reed-Sternberg cells
Transfusion Reactions
1. Acute Hemolytic Transfusion Rxn (major ABO incompatibility; high mortality)
2. Delayed Hemolytic Transfusion Reaction (slow progression destruction of RBCs)
3. Febril Reaction (donor white cells release inflammatory substances during storage)
4. Allergic rxn
Is preseptal cellulitis an orbital disease?
NO; it is inflammation of periocular structures (lids and skin) ANTERIOR to the orbital septum
Hordeolum dx and tx
dx: focal, painless, hard lump; blockage of glands of Zeiss or Moll
tx: hot compresses and topical and/or oral antibiotic like doxycycline or Keflex
Chalazion dx and tx
dx: meibomian gland blockage
tx: hot compresses; can be lanced or removed bc not infectious; if multiple get biopsied
Dacryocystitis dx and tx
dx: painful, swollen and infected lacrimal sac and/or drainage system
tx: oral antibiotics with a topical antibiotic such as a fluoroquinolone or even Polytrim; also give tylenol and codeine
*never lance bc do not want to spread infection
Clinical Presentation of Preseptal Cellulitis
1.mild orbital edema usually involving UPPER eyelid only
2. unilateral
3. warmth of eyelid
4. eyelid erythema, tho bulbar conjunctiva is white and quiet
5. **no proptosis, no EOM restrictions, and no pain on eye movement
6. globe is uninvolved
7. VAs and pupils are normal
Slit lamp evaluation of Preseptal Cellulitis
1. AC rxn
2. corneal/conj changes
3. s-shaped inflammation of upper lid
Tx of Preseptal Cellulitis
1. Tetanus toxoid: if traumatic
2. oral antibiotics: Keflex, Ceclor, Augmentin, Bactrim (if px is allergic to PCN), Erythromycin (if px is allergic to PCN and sulfa)
3. warm compresses
4. topical and oral decongestants
5. topical antibiotic: esp Polytrim or Polysporin
Is orbital cellulitis an orbital disease??
YES; an infection/inflammation within retrobulbar tissues within orbit; life threatening; px must be put on IV antibiotics; watch for exudative retinal detachment*
Etiology of Orbital Cellulitis
1. extension of preseptal cellulitis
2. **direct extension of sinus infection (#1 cause of orbital and preseptal)
3. following dacryoadenitis, dacrocystitis, acute hordeolum, chalazion
4. following orbital trauma, ocular foreign bodies
5. post-surgical
6. following a systemic illness like bacteremia or septicemia
Patient Symptoms/Signs of Orbital Cellulitis
1. Red, injected eye (*globe is now involved)
2. decreased VA or blindness: ON involved
3. Proptosis (key to dx!)- may cause double vision
4. malaise, fever, and headache- acute illness
5. *external ophthalmoplegia- inability to move eye
**3 Ps: Proptosis, external ophthalmoPlegia, Pain
6. possible APD (if ON is involved)
7. disc edema
8. fever
9. increased IOP
Tx of Orbital Cellulitis
IV antiobiotic to cross BBB
Forced Ductions (paresis vs mechanical involvement)
1. a paresis will move with forced ductions
2. mechanical involvement: eye will NOT move
Orbital Cellulitis with Cavernous Sinus Involvement
spread of infection of orbital cellulitis to cavernous sinus, leading to cavernous sinus thrombosis; fatal outcome
Clinical Presentation of Orbital Cellulitis with Cavernous Sinus Involvement
1. fever
2. progressive proptosis
3. BILATERAL**
4. EOM dysfunction
5. Rising IOP
6. Papilledema
7. Pain
*Remember 3 Ps: Pain, external ophthalmoPLEGIA, Proptosis
8. Purple lid skin
9. Severe congestion; bruit
10. fundus shows hemes, tortuosity, ON pallor
11. headache, nausea, vomiting, varying levels of consciousness
12. CN III, IV, and VI palsies
Orbital Cellulitis with Mucomycosis
life-threatening orbital FUNGAL infection; seen in diabetics, transplant pxs, and **severely immuno-compromised pxs
Dx and tx of Orbital Cellulitis with Mecomycosis
Dx: proptosis and EOM involvement, **black eschar: ischemic infarction and septic necrosis**; rapid deterioration
Tx:
1. Ketoconazole
2. Enucleation surgery
3. Amphotericin B to clean out hollow globe
4. Immediate hospitalization
5. Mortality rate: 30%
Idiopathic Orbital Inflammation
1. non-neoplastic, noninfectious space-occupying periocular lesion
2. may affect orbit focally, diffusely, or in a tissue-specific manner
3. 5% of all orbital lesions
4. may be acute, recurrent, or chronic
5. UNILATERAL*
6. males = females
7. peak incidence most frequently middle age
Signs/Symptoms of Idiopathic Orbital Inflammation
1. malaise and distress*
2. unilateral*
3. conjunctival chemosis and injection
4. uveitis
5. check vital signs*
6. sinuses are normal in CT scan* (in orbital cellulitis they are full of infectious material bc sinus infection is usually the cause)
7. no bony involvement of orbit*
Treatment of Idiopathic Orbital Inflammation *impt
trial of steroid therapy: 60 to 100 mg po once per day for 2 weeks to 1 month, with tapering dose over several months (also anti-ulcer meds, low dose radiation therapy, immunosuppressive agents, orbital biopsy)
Anterior Uveitis
inflammatory cells in the anterior chamber (ddx: HLA-B27, Bechet's, Sarcoidosis, Fuch's Heterochromic Iridocyclitis, JRA, Syphilis, Herpetic, Masquerade syndrome)
Intermediate Uveitis
inflammatory cells in vitreous
Posterior Uveitis
inflammtion of retina or choroid with or without vitritis
Panuveitis
all of above; entire eye involved
Limited Uveitis
duration of attack is <3 months
Recurrent Uveitis
>3 months between episodes
Chronic Uveitis
episodes <3 months apart, not including tx time
What test should be ordered with anterior uveitis?
HLA-B27
1. over 50% are HLA-b27 positive
2. 71% if unilateral and recurrent
3. 58% have seronegative spondyloarthropathy
What systemic disease has a high association with anterior uveitis?
Ankylosing spondylitis (45%)
-> 30-40% of pxs with AS will have at least 1 epidose of uveitis
Duration of tx for uveitis***
4-9 weeks per attack (mean duration 6 weeks)
Avg number of uveitis attacks***
Median = 3 (range 1-26)
Recurrent uveitis attacks can be associated with CME
Reiter's Syndrome (reactive arthritis)***
85-95% +HLA-B27
Triggers***:
1. Diarrhea or dysentery esp due to food poisoning
2. arthritis (usually within 30 days of infection)
Tx for Uveitis***
1. Topical corticosteroids for all **always use PRED FORTE
2. oral corticosteroids
3. periocular corticosteroids
How to taper steroids
only taper when there is a 2-step decrease in number of cells (= 1 grade level decrease)
Topical corticosteroids
for anterior disease
Periocular steroid injections
for unilateral, intermittent disease; CME
Oral corticosteroids
for bilateral, chronic, vision-threatening disease
Immunosuppressive drug therapy
steroid-sparing effect in chronic disease after steroids have been stopped
Differences between Episcleritis and Scleritis
Episcleritis
irritation
superficial inflammation
ocular complications uncommon
systemic disease uncommon
tx topical

Scleritis
painful
deep inflammation
ocular complications common
systemic disease common
tx systemically
What can you get in Wegener's Granulomatosis?
necrotizing scleritis
1. inflammation of small and medium sized blood vessels
2. scleral thinning
3. peripheral ulcerative keratitis
Diagnostic Tests for Scleritis**
1. always ddx syphilis & chest x-ray, RPR, FTA antibodies
2. ANCA C & P for Wegener's
3. Urinalysis
4. Chest x-ray
5. Lyme antibody
6. RF, ANA (rarely)
4 Connective Tissue Diseases
1. SLE
2. Scleroderma
3. Sjogren's
4. MCTD
Systemic Lupus Erythematosus (SLE)
1. 9 xs more common in women than men
2. 20-30 yrs
3. more common in AA, Hispanics, and Asians
4. autoimmune disease
Clinical Manifestations of SLE (DOPAMINe RASH)
Discoid rash
Oral ulcers
Photosensitivty
Arthritis
Malar rash: butterfly rash
Immunological: decreased WBC count
Neurological
Renal disorders
ANA +
Serositis +
Hematological: anemia, thrombocytopenia

**definite SLE: 4 or more criteria
Auto-antibodies tests for Lupus
1. Anti-dsDNA
2. Anti-Smith: specific for Lupus**
3. APLA
4. ANA
What is the most sensitive test for SLE?
ANA (97%) but has poor specificity
Tx of SLE
treat symptoms only:
1. NSAIDS for joints
2. High-dose glucocorticoids if severe and major organ involvement
DMARDS: disease-modifying agents
1. antimalarial druge
2. methotrexate: anti-neoplastic agent for disease control
Scleroderma
presence of thickened, sclerotic skin lesions; includes abnormalities of vasculature and involvement of multiple organ systems, **can often affect KIDNEY
Also:
1. peak ago of onset 30-40s
2. more common in females and AA
3. ***90% of pxs also have Raynaud's phenomenon
Clinical Manifestations of Scleroderma (CREST)
Calcinosis: calcium deposits in skin, nodules
Raynaud's Phenomenon
Esophageal dysmotility: trouble swallowing and acid reflux
Sclerodactyly: fibrosis of skin on fingers, long tapering thin fingers
Telangiectasia: small red blood vessels all over body

*scleroderma renal crisis: malignant HTN with renal failure is a medical emergency
Tx of Scleroderma
difficult to treat; no cure
1. D-penicillamine for skin disease
2. calcium channel blocker for Raynaud's phenomenon
3. ACE inhibitor for renal crisi
4. corticosteroids for pulmonary fibrosis
Sjogren's Syndrome
chronic inflammatory disorder caused by a lymphocytic infiltrate that destroys the lacrimal and salivary glands
Clinical Manifestations and Dx of Sjogren's
1. keratoconjuctivitis sicca, or KCS = dry eyes
2. Xerostomia (dry mouth)
3. 70% with +ANA, SS-S in 60-70%
4. + Schirmer test
Tx of Sjogren's
wetting agents, corticosteroids if severe symptoms, anti-malarial agents
Mixed Connective Tissue Disease (MCTD)
overlap syndome that has features of several connective tissue diseaes such as SLE, scleroderma
*characteristic antibody: Anti-RNP
Seronegative Spondyloarthropathies (SpA)
Features:
1.**more common in males than females (unusual for an autoimmune disease)
2. inflammatory back pain worse upon waking
3. peripheral arthritis (joints)
4. enthesitis (inflammation where tendons and ligaments attach to bone)
5. dactylitis (sweating and pain in fingers)
6. UVEITIS
7. sacroiliitis
8. spondylitis (vertebrae)
Ankylosing Spondylitis
1. male: female ratio of 4:1
2. 97% of AS px have HLA-B27
3. Get diarrhea after being infected with bug
4. predilection for sacro-iliac joints and spine (bamboo spine); px cant bend over and touch toes
5. elevated ESR
6. **Uveitis: acute, unilateral, recurrent
Tx of Ankylosing Spondylitis
1. exercise
2. posture training
3. NSAIDS
4. Sulfasalazine, Methotrexate
5. Anti-TNF agent: Etanercept***
Reiter's Syndome: Post-Infectous Arthritis or "Reactive Syndrome" Classic Triad
1. Urethritis
2. Conjunctivitis
3. Arthritis
Reiter's Syndrome
1. most cases occur within 1 to 4 weeks of dysenteric infection
2. 65-85% are HLA-B27+
3. Arthritis: 100% (predominantly of lower extremeties)
4. Enthesitis 70%
5. Dactylitis 20%
6. Spinal disease 20-30%
7. **Ocular: Uveitis (acute, unilateral and recurrent) and Conjunctivitis
8. **Urethritis (part of classic triad)
Tx of Reiter's
No good tx:
1. NSAIDS
2. Antibiotics for venereal infection
3. Sulfasalazine, Chloroquine, or Methotrexate
Psoriatic Arthritis
1. male:female ratio is 1:1
2. Often HLA-B27+
3. Arthritis: usually upper extremities
4. "sausage digits" dactylitis
5. extensive skin manifestations (scaly)
6. Tx: NSAIDS, Methotrexate, Cyclosporine, Etanercept, Infliximab, T-cell inhibitors: Efalizumab, Alefacept
Inflammatory Bowel Disease-Associated Spondyloarthropathy
1. can occur w/ Crohn's or Ulverative Colitis
2. oligoarthritis predominanly in lower extremities
3. sacroiliitis and spondylitis
4. uveitis**
5. HLA-B27 associated with #3 (but NOT peripheral arthritis
Bechet's Disease
1. small medium or large blood vessels
2. associated with HLA-B51
3. TRIAD***1) oral and genital ulcers, 2) uveitis, 3) arthritis
4. Skin: folliculitis, e. nodosum-like lesions 70%
5. tx topical steroids
Dx of Polyarteritis Nodosa
1. medium-sized vessel vasculities (ie vessels to heart)
2. joint inflmmation
3. cutaneous ulcers
4. mesenteric ischemia
5. dx: mesenteric or renal angiography showing microaneurysms, or biopsy**
Wegener's Granulomatosis
1. granulomatous vasculitis of small arteries, arterioles, and capillaries
2. Triad of organ involvement: upper respiratory tract, lungs, kidney
3. *necrotizing scleritis
4. dx + ANCA (antibody against own neutrophils)
5. tissue dx**: biopsy (sinuses or lung) = GOLD STD
6. tx: steroid & cyclophosphamide
Osteoporosis
1.common in elderly men with Vit D deficiency or post-menopausal women
2. **most common skeletal disorder in the world
3. bone mass value 1 to 2.5 SD below DEXA score = osteopenia
4. bone mass value 2.5 or more SD below DEXA score = osteoporosis
5. Type 1: Post-menopausal
6. Type 2: Senile (age-related)
7. dx with DEXA Scans (Dual Energy X-ray Absorptiometry): calculates bone mineral density
Prevention and Tx of Osteoporosis
Prevention:
1. calcium intake
2. Vitamin D intake
3. healthy weight
4. avoidance of ETOH, tobacco, and caffeine
Tx of Disease:
1. Calcitonin
2. Biphosphonates
3. estrogen
4. Fluoride
Most common joint disease?
Osteoarthritis
Osteoarthritis
-degenerative wear and tear
-NOT inflammation
-90% of pxs over ago 40
-causes: *obesity, wear & tear, previous inflammation, aging, genetic
Symptoms of Osteoarthritis
-joint degeneration but no systemic manifestation
-minimal morning stiffness
-pain
-crepitus
-warmth (will NEVER be hot)
Degenerative Changes in Osteoarthritis
early: narrowing of joint space
advanced: enzymatic degradation and thinning of cartilage
end stage: bones start touching/rubbing against one another
Three characteristic of Osteoarthritis (KNOW)
1) narrowing of joint space
2) osteophytes
3) bony cysts
Gout
-crystal deposition disease
-hyperuricemia (high uric acid levels cause crystals to form in joints)
Causes of Hyperuricemia (2)
1) under-excretion of uric acid
2) overproduction of uric acid
Acute Gout Attack
Podagra- big red inflammation of big toe
Polyarticular- involve multiple joints
Tx: resolves on its own
Which drug helps inhibit uric acid formation?
Allopurinol
When should allopurinol not be given?
during an acute gout attack bc it will make it worse
Which drug increases secretion of uric acid?
Probenecid
Pseudogout
Calcium Pyrophosphate Dihydrate Deposition (CPPD): NOT uric acid
Difference in crystals Gout vs Pseudogout
Gout crystals are needle-shaped and yellow
Pseudogout crystals are round and blue
Etiology of Infectious arthritis: Septic Arthritis **
Neisseria gonorrhea & Staphylococcus sp.

->rapidly destructive; can lost joints
Septic Arthritis: Dx
Arthrocentesis: important to culture bc if there is an infection, steroids are contraindicated!
What is an IgM marker for rheumatoid arthritis?
RF
How much is life expectancy decreased in RA?
3-18 yrs bc of disease and tx
Pathological hallmark of RA?
pannus (inflammation of tissues lining joints and is a systemic dx); inflammatory, proliferative synovial membrane (vs osteoarthritis which is not inflammatory and is limited to joints)
What is the leading cause of death in RA?
Coronary Artery Disease: due to inflammation of blood vessels
Tx of RA
NSAIDS
Steroids
DMARDS (Methotrexate, Hydroxychloroquine)
Antibodies
Aggressive early tx
Relapsing Polychondritis
episodic inflammation and destruction of cartilaginous structures and connective tissue (cartilage in EARS, nose, respiratory tract)
What is the gold standard for dx of Inflammatory Myopathies?
Muscle biopsy
Inflammatory Myopathies
cannot comb hair, cannot climb stairs
-polymyositis and dermatomyositis: inflammation of muscles with skin changes
-proximal muscle weakness(big muscles) and elevated CPK (muscle enzyme)
Tx of Inflammatory Myopathies **
Corticosteroids
Other immunosuppressants
IVIG: immunoglobulin
Physical therapy
Most commonly involved sites in Paget's Disease of Bone
**Skull
Sacrum
Spine
Femur
Tibia
Pelvis
Paget's Disease
abnormal bone remodeling: new weaker bone is formed, resulting in skeletal deformities and pain
What are the main symptoms of Paget's?
*bone pain and deformity
leg bowing
Tx for Paget's
analgesics
bisphosphonates to prevent bone resorption (Boniva)
surgery
NSAIDS
"Everywhere hurts"
Fibromyalgia
Most common cause of musculoskeletal pain in US in women 20-55 yrs
Fibromyalgia
DDx of Fibromyalgia
Depression, Chronic Fatigue Syndrome
What is the most common presenting symptom everywhere (in MD office/ER)?
acute back pain
What is the most common cause of acute back pain?
70% are lumbar strains and sprains
How do you treat acute back pain?
40% pxs are better in 1 week
90% pxs are better in 2 months
tell px to take NSAIDS and wait it out
What 4 things are most likely associated with carpal tunnel syndrome?
1) pregnancy, and women using oral contraceptives
2) Hypothyroidism
3) Diabetes
4) Dialysis pxs
Symptoms of Carpal Tunnel Syndrome
numbness and tingling in median nerve distribution; this nerve innervates thumb, pointer, and middle finger, and half of ring finger
Lateral epicondylitis
"tennis elbow"; involves extensor muscles of forearm and lateral epicondyle
Medial epicondylitis
"golfer elbow"; involves flexor muscles of forearm and medial epicondyle
Which muscle is most common torn in Rotator Cuff Tear?
supraspinatus tendon
What is the purpose of the rotator cuff?
to rotate and lift arm; stabilizes shoulder joint; a single tendon
Largest tendon in body?
Achilles Tendon
Most commonly ruptured tendon?
Achilles Tendon
Familial polypoosis coli
Colon cancer 100%
What is the most prevalent cancer in men?
prostate
What is the most prevalent cancer in women?
breast
What is the most common cause of death from cancer in men and women?
lung
Carcinomas arise from which type of cells?
epithelial cells
Sarcomas arise from what type of cells?
cells that make up bone or connective tissue
Leukemias and lymphomas arise from cells from where?
marrow/immune system
Which type of cancer does not have a reliable screening dx?
Lung cancer
Screening applies to which types of cancer?
cervix, breast, colon, prostate
TNM System
tells whether cancer is curable or not
Tumor: size, amt of local invasion? Label T1-T4
Node involvement: any/which ones? Label N0-N3
Metastasis: Yes/no? Label M0 for no, and M1 for yes
Does chemotherapy or radiation therapy damage nuclear DNA?
radiation therapy
What are the risk factors of breast cancer?
1. Increased age
2. 1st degree relatives afflicted (3x risk)
3. Genetics
4. Early menarche/late menopause
5. late first pregnancy or nulliparity
6. alcohol comsumption
Breast Cancer Tx
1. Surgery
2. Chemotherapy: all tumors >1cm
3. Hormonal Therapy: Tamoxifen: anti-estrogen drug
4. Biologic agents: Herceptin
5. Aromatase inhibitors: Arimidex, Femara *used only in post-menopausal women w/ HR positive tumors
American Cancer Society recommends colonoscopy when?
-beginning at age 50, every 10 yrs
-1st degree relative w/ cancer age >60: colonoscopy beginning at age 40, every 10 yrs
-1st degree relative w/ cancer age <60: colonoscopy beginning at age 40, every 5 yrs
Hereditary Non-Polyposis Colon Cancer (HNPCC)
when 3 1st degree relatives in 2 generations are diagnosed with colon cancer before age 50; almost everyone in family has some colon cancer
Tx for Colon cancer?
Hemicolectomy (removal of polyp) followed by chemotherapy
**Avastin is approved for metastatic colon CA and has minimal SE
How do you grade a tumor in prostate cancer?
Gleason score- a high gleason score is worse
Hormone Therapy for Prostate Cancer
LHRH (Luteinizing Hormone Releasing Hormone): agonist combined with testosterone receptor antagonist
When is chemotherapy used in prostate cancer?
only in refractory cases and widespread disease
What type of lung cancer is most aggressive?
small cell lung ca
What is the #1 risk factor for lung ca?
smoking
(also smoking + asbestos exposure)
Is adenocarcinoma more common in males or females?
females
Which type of lung ca is commonly found in smokers?
squamous cell carcinoma
aka oat cell carcinoma
small cell lung ca
Locations of adenocarcinomas, squamous cell carcinoma, and large cell carcinoma
adenocarcinoma: peripheral
squamous cell carcinoma: central lesions
large cell carcinoma: central
Where does lung ca often spread to?
bone and brain
Prognosis for lung ca?
poor; overall 5 yr survival is 10%
Is there a screening for lung ca?
NO
Gardasil
Vaccine to protect against cervical cancer; approved for 9-26 yr olds; effective against HPV 6, 11, 16, 18 (16 and 18 cause 75% of cervical CA)
Prognosis for Cervical Cancer
-94.6% survival at 5 yrs in early stages
-22% survival at 5 yrs in late stages
Risk Factors for testicular cancer
-undescended testis (*increased risk even with surgical correction)
-family hx
-infertility
-HIV infection
Survival Rate of testicular cancer?
one of most curable cancers; 5 yr survival exceed 90%
What should you never do on a testicular cancer px?
trans-scotal biopsy
What is done during orchidectomy in testicular cancer pxs?
retro-peritoneal lymph node dissection
ABCDs of skin lesions
Asymmetry
Borders: irregular
Color: not uniform
Diameter: larger
Major determinant of prognosis of skin cancer?
depth of tumor invasion
What are risk factors for cancer of the esophagus?
cigarettes and alcohol
Barrett's esophagus
change in epithelium over time with GERD: predisposes px to esophageal ca
Dx of esophageal ca?
CT of chest/abdomen: *look for enlarge lymph nodes
Prevalence of ovarian cancer?
affects post-menopausal women
What is associated with decreased risk of ovarian cancer?
early first pregnancy, multiparity, oral contraceptive use, breast feeding
Risk factors for Liver Cancer
*Cirrhosis (fibrosis of liver)
*Alcohol
*Hepatitis B and C
Should you dilate pregnant pxs?
every trimester with tropicamide only
What is the best glaucoma med for a pregnant px?
Propine (alphagan p is 2nd best)
What is a good rule of thumb for pregnant pxs?
No drops of any kind should be given! (do NCT, not goldmann, do no use proparacaine)
Is there an increase or decrease in BP in pregnant women?
decreased blood pressure
Dermatologic Changes in pregnant px
1. Chloasma: blotchy brown hypermelanosis that occurs around eyelids and fades post-partum; due to increased levels of MSH
2. Pre-existing nevi, freckles, and scars increase in size and pigmentation
3. Spider angiomas due to increased estrogen levels (abnormal change)
Visual function in pregnant px
-refractive errors remains constant**
-decrease in amplitude of accommodation in 2nd half of pregnancy (may need readers)
IOP in pregnant px
decreases
Pre-eclampsia
hypertensive disorder unique to pregnancy; after 20th week of gestation; overall edema of body
Eclampsia
same as pre-eclampsia PLUS seizures and/or coma
Symptoms of Eclampsia
*visual disturbances
*blurred vision
*30-100% have ocular symptoms
Hallmark retinal sign of Eclampsia
***focal retinal arteriolar vasospasm and narrowing
-also hemorrhage, exudates, CWSs, and eventually disc edema
Should you dilate pxs with PIH (pregnancy-induced hypertension)?
YES
Central Serous Chorioretinopathy (CSC)
spontaneous, localized serous retinal detachment (usually in area of macula)
Symptoms of CSC
**Metamorphopsia
-reduced VA
-micropsia
-dyschromatopsia
-refractive shift towards hyperopia
Clinical Manifestation of CSC
increased incidenve of gray or white subretinal exudates within the detachment (unique to pregnancy); presumed to occur due to fibrin in subretinal space
Purtscher-like Retinopathy
specifically related to child birth; occlusive vascular disorder; lack of blood flow to eye bc of retinal arteriolar occlusions during pregnancy
Funduscopic Findings in Purtscher-like Retinopathy
multiple, superficial, white retinal patches, resembling large CWSs, often associated with superficial peripapillary hemorrhages (right at disc); resolves spontaneously
Etiology of Disseminated Intravascular Coagulation
disturbance in homeostasis of body's clotting cascade
Disseminated Intravascular Coagulation occurs in:
-complicated abortions
-placental abruption; separation of placenta from uterus b4 baby is born
-pre-eclampsia
Clinical Manifestation of Disseminated Intravascular Coagulation
-widespread thrombus formation
-choroid most commonly involved
-serous retinal detachment due to occlusion of choriocapillaris
-fibrin deposition cause by clot formation in microvasculature
Funduscopic Findings of Disseminated Intravascular Coagulation
-choroidal hemorrhage
-cystoid macular edema
-serous retinal detachment
Amniotic Fluid Embolism
-occurs during labor, delivery, or in immediate post partum pd
-mortality rate in 80% range***
-embolic material within amniotic fluid deposits in microvasculature of heart, lung, brain, and eye
Symptoms of Pseudotumor Cerebri (PTC)
-increased intracranial pressure
-disc edema
-Paton's lines around ONH due to disc edema
-CN VI palsy
-visual disturbances
-headache, nausea, and vomiting
Visual Field of PTC patient
enlarged blind spot
Management of PIH
***immediate delivery of baby due to increased mortality risk of mother
Management of PTC
-weight loss
-Diamox, Naptazene
-**termination of pregnancy considered last resort (unlike PIH)
2 idiopathic miscellaneous disorders during/after pregnancy
1) ptosis
2) Idiopathic Facial Palsy (3x more likely during pregnancy)
Definition of CSME
1) exudates within 500 microns of foveola, if associated w/ adjacent retinal thickening
2) thickening of retina within 500 microns of foveola
3) zones of retinal thickening one disc area or larger, any part of which is within one disc diameter or foveola
Are pxs with gestational diabetes at risk for diabetic retinopathy?
NO- do not need to be dilated unless they have symptoms
What is a pathogenic mechanism for diabetic retinopathy?
increased retinal blood flow
Risk factors for progression of DR**
1. increased cardiac output
2. increased plasma volume
3. decreased peripheral vascular resistance
Category A Drugs during pregnancy
Controlled Studies show NO RISK
Category B Drugs during pregnancy
No Evidence of Risk in Humans; adverse findings in animals
Category C Drugs during pregnancy
Risk cannot be ruled out; human and animal studies are lacking
Category D Drugs during pregnancy
Positive Evidence of Risk; studies in humans have demonstrated fetal risk
Category X Drugs during pregnancy
Contraindicated in Pregnancy; studies have demonstrated positive evidence of fetal abnormalities or risk that clearly outweighs any possible benefit to px