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204 Cards in this Set

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2 types of EDEMA
Inflammatory
&
NON-inflammatory (NON white blood cells)
What are the 4 causes of edema?
1. Increased HYDROSTATIC pressure

2. Decreased PLASMA COLLOID osmotic pressure

3. Impaired LYMPH flow

4. RENAL retention of SALT & WATER (BIG AL & JG apparatus)
LOCAL AND GENERAL EFFECTS of increased hydrostatic pressure?
1. Local increases: impaired venous outflow (lower extremities) due to thrombosis/stasis = DEEP VEIN THROMBOSIS

2. Generalized increases: RIGHT SIDED HEART failure, RENAL failure and dysfunction.
3 states of disease/health that might cause a drop in plasma protein/colloid osmosis

(and therefore increase edema non-inflammatory)
NEPHROSIS - CIRRHOSIS - MALNUTRITION

all reduce plasma protein/albumin
What are 3 causes of LYMPHATIC obstruction?

*swelling cancer worm!
Inflammation
Neoplasia
Parasitic infection

(SWELLING - CANCER - WORM)
2 causes of SALT & WATER retention?
1. RENAL dysfunction due to atherosclerosis (JG apparatus & Big Al)

2. HEART disease (N-factor cannot get to kidney to tell it to dump H2o

**renin overproduction raises BIG AL, who raises BP which can increase the chance of edema b/c of hydrostatic pressure..
ATHEROSCLEROSIS IN RENAL ARTERIES CAUSES SAME THING.
DEPENDENT EDEMA
Cause?
Involves?
RIGHT SIDED HEART FAILURE
lower extremities involved, influenced by gravity - fluid has nowhere to go!
Peritoneal edema is also called?
KWASHIKOR'S or ASCITES
Cause of ANASARCA (GENERALIZED EDEMA)?


Anasarca is bad for your mascara and pantyhose...and you can't pee!
RENAL FAILURE = ANASARCA

*Anasarca is bad for your Mascara (periorbital edema) and Pantyhose (pitting edema of legs) and you can't pee (renal failure)!
PULMONARY edema & some presentations?
LEFT SIDED HEART FAILURE
Blood in lungs
EDEMATOUS AND PROTEINACEOUS
Drowning in blood
DYSPNEA
Why does BRAIN EDEMA occur?
How?
TBI

LOCAL or DIFFUSE.

VENTRICLES COLLAPSE, herniation results.
HYPER-EMIA vs. congestion
HYPEREMIA is NORMAL VASODILATION

congestion is pathological passive edema/swelling
Tell me about CONGESTION - Definition, cause, result?
PASSIVE CONGESTION is EDEMA (hyperemia does not cause edema - it is normal vasodilation. Congestion is a pathology)

DEPENDENT (heart) or ANASARCA/GENERALIZED (Renal)

Affected tissue becomes ISCHEMIC & CYANOTIC
Chronic/Passive congestion...

AFFECTED ORGANS (2)
why are each affected by passive congestion (non-inflammatory edema)
HEART-FAILURE CELLS IN LUNGS cause left sided heart failure

NUTMEG LIVER due to not being drained by right side of heart
What are 5 causes of a hemorrhage?

T.E.V.A.T.
TEVAT:
1. TRAUMA!!!
2. ANEURYSM
3. EROSION; microbes, neoplasia
4. VITAMIN deficiency
5. THROMBOCYTOPENIA (decrease in circulating platelets)
What is clinical significance of a hemorrhage dependent on?
HOW MUCH (VOLUME)
HOW FAST (RATE)
WHERE IS IT? (LOCATION)
hemoTHORAX
Blood in thoracic cavity
hemoPERICARDIUM
Blood around heart
hemoPERITONEUM
Blood in peritoneal cavity
hemARTHROSIS
Blood in joint capsule
Hematoma
NON-SPECIFIC bruise -small localized hemorrhage
PURPURA (purple all over)
Widespread bruising d/t metabolic imbalance
ECCHYMOSIS
Common skin bruise
PETECHIAE
Pinpoint hemorrhages tend to be in mucous membranes.
What is hemostasis?
CLOT FREE LIVING UNLESS NEEDED:
Maintenance of clot-free blood w/in the vascular system while allowing for the formation of a solid plug of blood under conditions of vessel wall injury.
HEMOSTASIS key players (3)
VASCULAR ENDOTHELIUM

PLATELETS

COAGULATION SYSTEM
INTACT endothelium

INHIBITS CLOTTING/PLATELET AGGREGATION by...(4)
1. INSULATES/PROTECTS PLATELETS from subendothelial collagen

2. PG12 (PROSTACYCLIN)

3. ADPase synthesis

4. NITRIC OXIDE for VASODILATION
HEPARIN
ANTI-THROMBIN III (degrades thrombin)

STOPS CLOT by removing thrombin
FIBRINOLYTIC activity of ENDOTHELIAL CELLS (form endothelium)
TISSUE PLASMINOGEN ACTIVATOR (t-PA)
converts plasminogen to plasmin (plasmin degrades fibrin)

Decreased activity leads to hypofibrinolysis which can result in thrombosis or embolism.
How does damaged endothelium ATTRACT CLOTTING ?
1. von WILLENBRAND'S FACTOR synthesis

2. TISSUE FACTOR synthesis

3. PLATELET-ACTIVATING FACTOR synthesis

4. T-PA (tissue plasminogen activator) INHIBITOR synthesis
VON WILLENBRAND'S FACTOR
PLATELET ADHESION

There are mild, moderate and severe von Willebrand's disease which are bleeding diseases where can't fuse clots where needed. Can cause infertility
SIGN: HEAVY MENSES
TISSUE FACTOR
A glycoprotein which
ACTIVATES COAGULATION
system.
PLATELET-ACTIVATING FACTOR makes platelets ________
STICKY!!
TPA gets inhibited, then what?

As an enzyme, TPA (tissue plasminogen activator) catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown.

(TISSUE PLASMINOGEN ACTIVATOR inhibited)
If no TPA, then the clot is NOT BROKEN UP

TPA: As an enzyme, it catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown.

no Tissue Plasminogen Activator so clot not degraded

Because it works on the clotting system, tPA is used in clinical medicine to treat ONLY EMBOLIC or THROMBOTIC STROKE! Use is contraindicated in hemorrhagic stroke and head trauma.
BRICKS of a thrombus
PLATELETS = BRICKS
PLATELETS OPPOSE the actions of the _________
ENDOTHELIUM


(platelets vs. endothelium)
What is SECRETED by platelets to ACTIVATE them?

58F.A.T.Cows
58FATCows:

Factors 5 and 8

ADP

Thromboxane (TXA2)

Ca+
BINDS to EXPOSED COLLAGEN
von WILLENBRAND factor
ACTIVATED PLATELETS start the ___________ cascade
ACTIVATED PLATELETS play a role in ____+ and __________ complex.
COAGULATION cascade

Ca+ and PHOSPHOLIPID complex
TEMPORARY PLUG changes to DEFINITIVE when...
FIBRIN forms from thrombin (precursor) = FUSED MASS of PLATELETS
3 steps of the COAGULATION process when ENDOTHELIUM (lining) is damaged...
1. FACTOR XII or TISSUE FACTOR III arrives

2. NET of FIBRIN via trapping/polymerizing a woven net

3. CEMENT FIBRIN = (fibrin, platelets, RBCs and WBCs)

*TISSUE FACTOR III aka thrombokinase: initiation of thrombin formation from the zymogen prothrombin.(vs TPA which converts plasminogen to plasmin to break up a clot)
THROMBOSIS
(3)
1. An aggregate PLATELETS/FIBRIN/RBC'S in a non-interrupted vascular system

2. BINDS/ADHERES to the vascular endothelium (vs a post-mortem clot)

3. may be EITHER ARTERIAL or VENOUS
What are 3 predisposing factors to arterial thrombi?
1. Damage to endothelium 2. Alterations in normal blood flow 3. Increased coagulability of blood
ENDOTHELIUM/LINING of lumen injury (5 causes)
1. ATHEROSCLEROSIS (McDonald's)

2. HEMODYNAMIC stress (high blood pressure!)

3. RADIATION/TRAUMA/CHEMICALS/MICROBES (risks of living)

4. ISCHEMIA of ENDOcardium (no blood, no go!)

5. VALVE DAMAGE (filter stenosis)
STASIS & TURBULENCE results/problems
1. PHYSICAL DAMAGE to endothelium

2. DISRUPTS LAMINAR flow

3. PREVENTS RENAL CLEARANCE of COAGULATION proteins

4. rRETARDS ANTICOAGULANT FLOW to site of injury
What are 5 causes of INCREASED coagulability of blood?

i.e., who's gonna throw a clot?
1. GENETIC defect in anticoagulant proteins or coagulant proteins

2. HOMOCYSTEINE

3. NEOPLASIA - release of procoagulants

4. POLYTHYMIA VERA (RBC neoplsia)

5. SMOKING, OBESITY
What are the 3 MOST COMMON ARTERIAL THROMBOSIS SITES;

and what is the result?
1. Coronary ARTERY
2. Cerebral (stroke) ARTERY
3. Femoral ARTERY

ISCHEMIC INFARCTION = loss of blood supply
ARTERIAL THROMBUS DEATH TERMs
INFARCTIONS!
caused by artery thrombus

MYO/CARDIO infarct of an ARTERY
CEREBRAL infarct of an ARTERY
RENAL infarct of an ARTERY
4 types of VENOUS thrombosis
1. VARICOSE VEINS
2. DEEP LEG VEINS
3. RED thrombi due to CYANOSIS
4. PHLEBO-thrombosis
lines of ZAHN
GROWTH RINGS ON A THROMBUS, LIKE A TREE


Start/stop growth pattern w/in a thrombus, shows that thrombus is growing and chronicity of thrombus in a vessel
Thrombus ATTACHED TO THE WALL of the HEART

What are possible sequelae of these _______ THROMBI?

The thrombotic material may break off and go to the brain or kidney (the two most likely sites since they get so much blood flow) or any arterial system
MURAL THROMBUS

Why do mural thrombi form on the endocardium of the heart after a myocardial infarction?
The infarct produced necrosis and inflammation. Also, the infarcted ventricular wall is akinetic and/or dyskinetic (bulges outward during systole). Thus, the blood in the ventricle tends to form thrombi on the surface of the infarcted endocardium
How can you tell it's a POSTMORTEM clot?
NOT ADHERENT TO VASCULAR WALL

Blood stasis following death
HAIR LIKE, FINGER LIKE, WART LIKE GROWTHS
DUE TO INFECTIVE ENDOCARDITIS
VEGETATIONS on HEART VALVES
due to OLD BACTERIAL INFECTION

RHEUMATIC FEVER;


heart valves associated w/ bacterial infection of heart consequence of rheumatic fever (cardiac sequelae) upon 2nd exposure untreated sequelae reaches 50% -> murmur, defect, arhythmias.
VERRUCOUS (Libman Sacks) Endocarditis?
LIBMAN SACKS ARE VERRUCOUS
Produce vegetations NOT DUE TO bacteria!
manifestations of DVTs?
PULMONARY EMBOLIZATION

Edema of foot and ankle,
pain of foot and ankle
(Homan's sign = broad hand on gastroc.), "HO, MAN! THIS HURTS!"
local ischemia - bacterial skin infections,

PULMONARY EMBOLIZATION
What are the 4 potential fates of a thrombus?
1. Dissolution 2. Propagation 3. Organization 4. Recanalization
ORGANIZATION & RE-CANALIZATION of thrombus
Phenomenon of permanence of a clot; increase in blood flow is variable, attempt to increase amount of blood flow. Recanalization forms thru channels by migration of endothelial cells w/in body of clot, added flow thru clot
THE WORST POSSIBLE FATE
EMBOLIZATION :-(

detaches from vascular wall and travels downstream,
(MC: THROMBO-EMBOLUS) until hits smaller diameter vessel ->

INFARCTION!!! with partial or complete occlusion of vessel lumina.

PULMONARY = VENOUS
SYSTEMIC CIRCULATION = ARTERIAL
EMBOLISM def.
DETACHED
INTRAVASCULAR MASS

BLOOD BORNE TO SOMEWHERE FAR, FAR AWAY
What is thromboembolism and what is the result?
MC = thromboembolus results in partial or complete occlusion of vessel lumina, may lodge in pulmonary or systemic circulation.
THREE WHOOPS! - THROMBOEMBOLI types of subcategories (bad luck)
1. FAT from FEMUR FRACTURE

2. AIR from THE BENDS (diving)

3. AMNIOTIC from PLACENTAL TEAR sucked into systemic circ. sucks up amniotic fluid -> TOXIC!
Discuss pulmonary emboli as a case scenario.
PREVENTABLE DEATH in hospitalized pts

use AMBULATION & ANTICOAGULANTS

arise from DVT,

small vs. large emboli.
SADDLE embolus
saddle-shaped EMBOLUS that
wedges at the BIFURCATION OF A PULMONARY TRUNK
and BLOCKS BLOOD TO LUNG.

SHOCK results
SYSTEMIC emboli come from which side of the heart?

*remember the difference b/w pulmonary and systemic supply; one is vein, the other is artery
SYSTEMIC EMBOLI = ARTERIAL

LEFT VENTRICLE w/ ruptured atherosclerotic PLAQUES
Where do SYSTEMIC (arterial) EMBOLI get STUCK? (3)
1. LOWER EXTREMITIES (75%)
-> acute infarction -> sudden gangrenous necrosis

2. BRAIN (10%)

3. VISCERA (10%)
INFARCTION def.
ISCHEMIC AREA OF NECROSIS

DUE TO THROMBUS OR EMBOLUS BLOCKING BLOOD SUPPLY TO ORGAN OR TISSUE

results: HEMORRAGE or ISCHEMIA/NECROSIS and edema
INFARCTS are ________-shaped.

2 TYPES (COLORS)
WEDGE-shaped!

WHITE INFARCT = THROMBOEMBOLUS (paling of area)
vs.
RED INFARCT = HEMORRAGIC (reddening of are due to bleed out of vascular wall into tissue)
FACTORS determining an INFARCTION
VASCULAR SUPPLY (is it good, bad? nature of it)

RATE OF DEVELOPMENT of occlusion

VULNERABILITY of that tissue to HYPOXIA
i.e. heart very, skin not so vulnerable
MORPHOLOGY of an INFARCT
WEDGED

INFLAMMED HYPEREMIC MARGINS

FIBRINOUS EXUDATE covering surface due to CLOTTING FACTORS

COAGULATING NECROSIS/DEATH of CARDIAC mm.
HEMODYNAMIC SHOCK
HYPOPERFUSION

DECREASED BLOOD TO ALL TISSUES

!st series of changes are REVERSIBLE
2nd series of changes are not.
HEMODYNAMIC subtypes of shock? (5)

Neurotic Voles Avoid Cardiac Snakes' blood
Neurotic Voles Avoid Cardiac Snakes' blood so they don't go into shock!

1. CARDIOGENIC
2. HYPOVOLEMIC
3. SEPTIC
4. ANAPHYLACTIC
5. NEUROGENIC
(result from SC injuries, vasomotor responses altered, ANS - HR, vascular tone affected.
CARDIOGENIC SHOCK
HEART PUMP FAIL COMPLETE
How would an MI cause CARDIOGENIC SHOCK?
ACUTE LOSS TO VENTRICULAR WALL = DEATH
CARDIOGENIC SHOCK due to CARDIAC TAMPONADE

One of the most common settings for cardiac tamponade is in the first 24 to 48 hours after heart surgery. After heart surgery, chest tubes are placed to drain blood. These chest tubes, however, are prone to clot formation. When a chest tube becomes occluded or clogged, the blood that should be drained can accumulate around the heart, leading to tamponade
BREACH!
FLUID POURS INTO PERICARDIAL SAC AND COMPRESSES HEART.

LOW STROKE VOLUME B/C ventricle can't pump.
Can be d/t cocaine abuse or klenbuterol.
COR PULMONALE as a type of cardiogenic shock

*pretend it says Coeur Pulmonale' ~ now what two organs are involved?
SADDLE EMBOLUS BLOCKS BRONCHUS

NO BLOOD TO LUNGS SO NO OXYGEN TO BODY

HEART BEATS LIKE CRAZY, THEN UP AND QUITS
HYPOVOLEMIC shock
subtype of hyperemic:

BLOOD LOSS ~ BLEED OUT ~ TANK BLOOD PRESSURE
What are causes of hypovolemic shock?
BLOOD PRESSURE CRASH SHOCK
Hemorrhage, severe trauma, extensive burns (weep blood plasma -> infection and hypovolemic shock; BP hard to maintain.
SEPTIC SHOCK
BACTERIAL ENDOTOXINS CAUSING SHOCK/SEPSIS:

GRAM-NEGATIVE bacteria ->

TOTAL VASODILATION DUE TO INFLAMMATORY MEDIATIORS

THEN, TOTAL VASOCONSTRICTION = BLOOD PRESSURE CRASHES!
What is the pathophysiology of SEPTIC SHOCK? (3)
ENDOTOXINS FROM GRAM NEG. bacteria,

CYTOKINE RELEASE (IL-1, 6 & 8, TNF),

cytokines trigger PA Factor , NO, bradykinin, complement, protaglandins, leukotrienes
STAGES of SHOCK
NON-PROGRESSIVE

PROGRESSIVE

IRREVERSIBLE
NON-PROGRESSIVE SHOCK
COMPENSATORY MAINTENANCE of BP =

ANS,
SNS,
Renin-angiotensin-aldosterone axis,
autoregulation.
PROGRESSIVE stage of shock


*turning blue after dropping acid @ a progressive rock concert
HYPOXIA tissue (turning blue)

ACIDOSIS metabolic (after dropping acid)
IRREVERSIBLE shock stage
ENZYME LEAKAGE EVERYWHERE
ORGAN FAILURE
MASSIVE TISSUE DEATH
What does the tunica intima of blood vessels provide and what is it composed of?
Provides interface b/w blood and tissues; composed of vascular endothelium which possesses important multifunctional and metabolic properties.
What are the functions of the tunica intima?
Semi-permeable membrane, maintenance of non-thrombogenic blood-tissue interface, modulation of blood flow and vascular resistance, regulation of immune and inflam. reactions,

GROWTH REGULATION OF OTHER CELLS - ESP SMOOTH MUSCLE CELLS
What can endothelial cells do based on stimuli?
CHANGE THEIR BEHAVIOR

"ENDOTHELIAL ACTIVATION!"
INCDUCERS of ACTIVATION for ENDOTHELIAL CELLS: (7)
ANYTHING THAT CAN DAMAGE THE ENDOTHELIUM OR AFFECT IT:

CYTOKINES
BACTERIA
HEMODYNAMIC STRESS
LIPIDS
VIRUSES
COMPLEMENTS (they are bashful)
HYPOXIA
ACTIVATED endothelial cell PRODUCTS:
ADHESION MOLECULES

CYTOKINES

CHEMOKINES

GROWTH FACTORS

VASO-ACTIVE MOLECULES
ACTIVATED ENDOTHELIAL CELLS can...
VASOCONSTRICT OR VASODILATE

PRO- OR ANTI-COAGULANTS

RELAXING OR CONTRACTING FACTORS to calm SMOOTH MUSCLE SUBENDOTHELIAL environment
What causes arterioclerosis?
Endothelial activation and subsequent pathological changes.
What are the 3 DISTINCT PATTERNS of arteriosclerosis?
ATHEROsclerosis (MOST clinically significant)

MONKEBERG MEDIAL sclerosis (CALCIFIC deposits in muscular aa.)

ARTERIOclerosis (affects SMALL arteries and arterioles: related to metabolic and autoimmune diseases, diabetes mellitis)
ATHEROSCLEROTIC ARTERY SIZE(S) & TYPE
ELASTIC
LARGE & MEDIUM MUSCULAR TYPES
ATHEROSCLEROSIX:
1 -INITIAL
2- FATTY STREAK
3- INTERMEDIATE
3- ATHEROMA
4- FIBROATHEROMA
5. it's COMPLICATED
ATHEROSCLEROSIX type #1 progression?
First atherosclerotic lesion,

isolated MACROPHAGE FOAM CELLS by age 4-5
ATHEROSCLEROSIX #2
#2 FATTY STREAK

INTRACELLULAR lipid accumulation (the blush of fat is, well, yellow)
ATHEROSCLEROSIX #3


Initial - Fatty streak - Intermediate - Atheroma - Fibroatheroma - it's Complicated
#3 INTERMEDIATE (RIGHT BEFORE AN "OMA")...


FATTY STREAKS W/ LIMPID POOLS (lipid pools) extracellularly
# 4 ATHEROSCLEROSIX progression?

Initial - Fatty streak - Intermediate - Atheroma - Fibroatheroma - it's Complicated
#4: ATHEROMA is...

FATTY STREAK (#2) and CORE of extracellular LIPID

*since it is an "oma," it must have a core of something like a tumor and look like fat on the outside since we are talking atherosclerosis/cheese burgers
ATHERSCLEROSIX #5
#5 FIBROATHEROMA:

CALCIFIC, FIBROTIC LIPID CORE AND FIBROUS LAYERS
ATHEROSCLEROSIX #6
#6 it's COMPLICATED

SURFACE DEFECT
HEMATOMA
HEMORRAGE
THROMBUS

*Symptoms all depend on the size of the thing.
CLINCIAL EVENT HORIZON = WHAMMO!
What is the BASIC PROGRESSION of atherosclerosis?
Normal (INITIAL) -> FATTY STREAK (then intermediate, then) -> ATHEROMA -> larger atheroma -> COMPLICATED lesion S/S clinical event horizon. THEN WHAMMO!
What are 7 risk factors associated with atherosclerosis?
1. hypertension 2. hyperlipidemia 3. smoking 4. sex 5. diabetes 6. "soft risks" sedentary, stress, obesity 7. "new risks" hinge on infective process
Why can hypertension cause atherosclerosis?
alterations in blood flow
Which sex is initially at higher risk of developing atherosclerosis?
Males, post menopausal females catch up.
What sort of risk for atherosclerosis does diabetes cause?
Greatest risk, uncontrolled glucose [] in blood -> endothelial cell harm
What are 2 lesions of atherosclerosis?
1. Fatty streaks: early intimal lipid accumulation 2. Atheromatous plaques: raised subintimal plaques of necrotic tissue, lipid, ECM and cells
What are 4 theories of pathogenesis of atherosclerosis?
1. Response to injury hypothesis 2. Monoclonal hypothesis 3. Hemodynamic hypothesis 4. Infective hypothesis
What is the response to injury hypothesis of atherosclerosis?
Endothelial cell dysfunction/activation -> macrophage involvement -> smooth muscle cell involvement -> hyperlipidemia. Or, injury, response and degenerative changes lead to atherosclerotic plaque.
What do macrophages do when involved with atherosclerosis?
Ingest lipid to produce foam cells, oxidatively damage LDL (form free radicals), recognize damaged LDL (consume damaged LDLs -> form free radicals -> collateral damage), release chemical mediators = chemoattractants and mitogens.
What occurs with smooth muscle cell involvement of atherosclerosis?
Proliferation of VSM contributes to growth of lesion: role of growth factors PDGF, FGF, deposition of ECM contributes to growth of lesion. Picture pg. 35
What is the mechanism of lesion progression with atherosclerosis?
Persistent endothelial cell dysfunction -> persistent inflammation -> persistent hyperlipidemia -> ?persistent homocysteinemia, bacterial infection, vitamin deficiencies. picture pg. 36
What makes up a firbrous cap?
smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularization.
What makes up the necrotic center of an atherosclerotic lesion?
cell debris, cholesterol crystals, foam cells, calcium
What are 4 possible resulting lesions of atherosclerosis?
1. Ulceration 2. Thrombosis 3. Hemorrhage 4. Calcification
What are 4 clinical manifestations of atherosclerosis?
1. Acute occlusion (MI) 2. Chronic narrowing (-> stenosis; atrophy of downstream organ) 3. Aneurysm formation 4. Embolism
What is an aneurysm?
A localized dilation of a blood vessel or chamber of the heart.
What are the 5 most common sites of aneurysms?
1. Aorta 2. Iliac 3. Splenic 4. Renal 5. Vertebral
How would a patient present with lumbar artery occlusion?
Constant LBP that won't resolve with manipulation.
What are 2 broad categories of aneurysms?
True: where the aneurysm is bounded by arterial wall components, all 3 layers outpouch. False: Where a breach in the vasclar wall leads to a vascular hematoma, 1 or more layers -> hemorrhage into other layers creating a false lumen.
What are 4 causes of a True Aneurysm?
1. MC: Atherosclerotic 2. Syphilitic 3. Congenital 4. Left ventricular
What are 3 causes of a False Aneurysm?
1. MC: Post myocardial infactive 2. Junctional leak at vascular graft 3. Genetic (Marfans)
What types of aneurysms are there?
2, true and false
What are the morphologies of aneurysms?
shape
What are the etiologies of aneurysms?
what causes particular aneurysm
What are 4 morphologies of an aneurysm?
1. Berry 2. Fusiform 3. Saccular 4. Dissecting
What is a berry aneurysm?
Very small spherical dilations, occur most frequently at brain base, circle of willis, congenital, asymptomatic.
What is a saccular aneurysm?
5-10 cm. in diameter spherical dilations whose mechanism is wide and variable.
What is a fusiform aneurysm?
Gradula and progressive dilation of a blood vessel producing a spindle-shaped expansion. May be eccentric (unilateral) or bilateral. Etiology typically atherosclerotic.
What is a dissecting aneurysm?
False aneurysm; refers to escape of blood into the tunica media, "double barrel" presentation of lumen, dialtion of blood vessel doesn't need to exist for this type to occur. 2 types.
What are the 2 types of dissecting aneurysms and what is the etiology?
Type A (arch of aorta) and Type B (descending aorta). Both present with breach in vascular wall and generation of false lumen. Etiology: genetic: Marfans
What is a pseudoaneurysm?
Not false. Traumatic injury to muscle layer producing focal dilation. Also referred to as traumatic aneurysm or post traumatic aneurysm.
What are 6 classifications of aneurysm by etiology/location?
1. Atherosclerosis: MC -> fusiform (true) usually AAA. 2. Infection (sepsis) 3. Post stenotic dilatation 4. Syphillis 5. Arteritis 6. Miscellaneous (congenital)
Who is most likely to get an atherosclerotic aneurysm, when is it diagnosed and how does it present?
MC is AAA Men more often than Female (60-80 y/o) Dx'ed when more that 50% dilation of normal diam. of vessel has occurred. Associated w/ hypertension and heart disease Intermittent back/abdominal pain Claudication Lower limb ischemia
What is the difference b/w neurogenic and vascular claudication?
Neurogenic: pain with walking is always present Vascular: Pain after walking a while, starts to throb b/c muscle needs more blood.
What does aneurysm size have to do with its chance of rupture?
If <5 cm there is <5% chance of rupture If >6 cm there is ~15% chance of rupture If >7 cm there is 75% chance of rupture
What must treatment of an aneurysm account for and consist of?
Must account for risk/benefit of surgical intervention. Consists of removal of dilation and replacement w/ graft.
What are 2 non inflammatory vascular disorders?
1. Monkeberg medial sclerosis 2. Raynaud phenomenon
What are 8 inflammatory vascular disorders?
1. Takayasu arteritis 2. Polarteritis nodosa 3. Allergic granulomatosis and angitis (Churg-Strauss) 4. Temporal arteritis (giant cell arteritis) 5. Kawasaki disease 6. Wegeners granulomatosis 7. Thromoangitis Obliterans (Buerger's) 8. Behcet
What is Monkeberg medial sclerosis?
A degenerative calcification of the tunica media of large and medium sized muscular arteries, typically older individuals, MC in aa. of extremities (non-elastic), no luminal narrowing, unknown etiology.
With Monkeberg medial sclerosis what is a presentation that may appear on an x-ray?
"Pipe-stem calcification"
What is Raynaud Phenomenon?
Typically d/t cold induced vasoconstriction, Fingers change color in sequence white-blue-red, exaggeration of normal central and vasomotor responses to cold or emotion, usually benign, ulceration and gangrene rare, may be primary or secondary
What is inflammatory vasculitides?
Refers to inflammation of the walls of vessels (any type or size) and its effect. Can be classified based on pathogenesis/etiology, infection, immunologic. (Picture pg. 50)
What are clinical presentations and treatments of inflammatory vasculitides?
Often a result of affected vessel lumen narrowing/obliteration/dilation/thrombosis. D/T their nature vasculitides are steroid/immunosuppressive therapy responsive.
What is Takayasu arteritis, who is affected and where is it?
Females <40, involves aortic arch, may involve branches, Charac. principally weakening of peripheral pulses, Exam shows thickening of aorta, esp. aortic arch and branches w/ near obliteration of distal portions of branches.
What would you expect to find upon examination of a patient with takayasu arteritis?
Higher BP on one side vs. the other Pulse and BP disparity
What is polyarteritis nodosa?
Necrotizing vasculititis of small and medium sized visceral arteries with NO LUNG INVOLVEMENT
How does polyarteritis nodosa present?
Young males, present with necrotizing of vessel wall (fibrinoid necrosis). If affects small aa. may be associated with Perinuclear Anti-neutrophil Cytoplasmic antibody (P-ANCA)
In what 3 phases can polyarteritis nodosa present?
Acute, healing, scarred (may co-present)
What are complications of polyarteritis nodosa and what is it usually responsive to?
Aneurysm, thrombosis, infarct; corticosteroid responsive
What is Allergic granulomatosis and agnitis (Churg-Strauss)?
Systemic vasculatis in young individuals with asthma, 2/3 patients have C-ANCA or P-ANCA, small and medium sized aa. and arterioles of lungs, spleen, kidney, heart, CNS (visceral complaint), shows intense eosinophilic infiltrate.
What is giant cell arteritis (temporal arteritis)?
>50 y/o, MC systemic form of vasculitis in adults, both acute and chronic, affects lg. and sm. aa., esp. temporal aa. also vertebral and ophthalmic.
What is the pathogenesis of giant cell arteritis?
Suggests that immune reaction is generated towards components of the vascular wall - still putative; Granulomatous nature suggests t-cell mediated mech. and antigen-driven injury.
What are clinical features of temporal arteritis?
Facial pain, intense w/ palpation, ocular symptoms, can lead to sudden, permanent blindness, tx w/ anti-inflammatory.
What is Kawasaki disease?
Disease of the coronary arteries, affecting young children <4 y/o. Unknown etiology. Associated w/ mucocutaneous lymph node syndrome. 20% develop cardiac sequelae...aneurysmal formation.
What are clincial consequences of kawasaki disease?
Asymptomatic vasculitis, coronary artery ectasia (non-aneurysmal dilation), Thrombosis, MI, sudden death.
What treatment is given for kawasaki disease?
Aspirin megadoses and intravenous gammaglobulin (gets immune system to fight)
What is Wegener's granulomatosis?
Necrotizing vasculitis characterized by triad: 1. Acute necrotizing granulomas of upper respiratory tract 2. Necrotizing granulomatosis of small to medium sized vessels 3. Renal disease in form of focal glomerulitis (type 4 like)
What are some other facts about Wegener's granulomatosis?
Pathogenesis suggests some type of hypersensitivity rxn. 90% present w/ ANCA where 75% is C-ANCA. Rapidly fatal if not treated. Tx w/ cyclophosphamide (chemo agent).
What is Thromboangitis obliterans (Buerger's disease)?
Distinctive disease leading to vascular insufficiency. Segmental acute and chronic thrombosis of small and medium aa. Microabscesses/granulomatous inflammation.
What are the principal arteries affected with Buerger's disease and who gets it?
Tibial and Radial aa. Almost exclusively in heavy smoking men who present with symptoms of claudication, cold intolerance/Raynauds. Lumen obliteration w/ distal necrosis.
What is Behcet?
Mainly involves mucous membranes, charac. by oral apthous ulcers, genital ulceration, ocular inflammation and lesions in CNS, heart and GI. Unknown cause, immune basis, tends to not be as severe.
What are varicose veins?
Enlarged tortuous blood vessels from increased intraluminal pressure, affects women>men, familial predisposition, obesity and prego plays a role. Walls may be thinned d/t dilation or thickened d/t hypertrophy. Stasis dermatitis and secondary ulceration
Where may VARISCOSITIES besides the LEGS?
Rectum and anus: hemorrhoids
Esophagus: esophageal varices, enlarged v in esophagus d/t hepatic diseases MC cirrhosis/liver Clinically silent until tear occurs and bleeding event depends on how bad liver cirrhosis is. Scrotum
What is thrombophlebitis?
Thrombotic condition of veins that implies inflammation present.
What is Phlebothrombosis?
Thrombus in vein, inflammation not implied.
What is DVT associated with and what are some symptoms?
Prolonged bed rest, reduced cardiac output, surgery. General swelling in calf, ankle, foot or thigh, increased warmth of leg, redness, pain in leg, night leg cramps, bluish discoloration of skin on legs or toes.
What is the cause of death w/ DVT and what is a treatment?
Pulmonary embolus resulting in cor pulmonale Caval filter
What are benign hemangiomas?
Neoplasia of capillaries. common congenital vascular lesions, MC on skin but also found on mucosal surfaces and visceral organs, lesions present at birth and grow but limited in size.
What are capillary hemangiomas?
Vascular channels have the size and strx of normal capillaries, occur on skin (strawberry hemangioma) subcutaneous tissue, mucous membranes of mouth and lips. Strawberry hemangiomas fade at 1-3 y/o.
What are cavernous hemangiomas?
Lesions consist of large vascular channels, port wine stains, raised spongy masses that do not regress spontaneously, may undergo thrombosis, fibrosis, hemorrhage. Significant in von Hippel Landau disease
What is angiosarcoma?
rare highly malignant consists of neoplastic endothelial cells, located on skin, soft tissue, breast, bone, spleen, liver. Varying degrees of differentiation. Liver involvement associated w/ carcinogens: vinyl chloride, arsenic, thorotrast
What is Kaposi's sarcoma?
Derived from neoplastic endothelial and stromal cells, associated with AIDs, painful, purple/brown nodules/plaques on hands, feet, face. Rarely primary cause of death.
What occurs with a coronary artery bypass?
Vein or artery grafts long term patency grafts subjected to thrombosis, intimal thickening, atherosclerosis.
What is throbolysis?
Tx to lyse thrombi and emboli (leg vein thrombi, pulmonary emboli, prosthetics, catheters) plasminogen activators used. Problems: falure to lyse, reocclusion d/t persistence of orginal disorder.
What is balloon angioplasty?
Luminal expansion of atherosclerotic arteries, atherosclerotic plaque becomes unstable, complications: plaque rupture, medial dissection, stretching of the media (exposure of collagen), proliferative restenosis
Blood pressure is maintained by the force generated by a pump =
heart
Blood pressure: the _________ in the distribution system (the arteries), and the amount of intravascular fluid.
resistance
Resistance is related to the ____ of the arterial bed. At the arteriole level, opening and dilating arterioles reduces pressure.
size
Blood pressure is maintained by the force generated by a pump (the heart), the resistance in the distribution system (the arteries), and the amount of intravascular fluid. Resistance is related to the size of the arterial bed. At the arteriole level, opening and dilating arterioles reduces pressure.
The system requires pressure monitors. The kidney contains mechanisms to control blood pressure. When the glomerular filtration rate (GFR) drops, the stretch receptors in the macula densa signal cells of the juxtaglomerular apparatus to secrete renin.
The system requires pressure monitors. The kidney contains mechanisms to control blood pressure. When the _________________________ drops, the stretch receptors in the macula densa signal cells of the juxtaglomerular apparatus to secrete renin.
Glomerular Filtration Rate (GFR)
The system requires pressure monitors. The kidney contains mechanisms to control blood pressure. When the glomerular filtration rate (GFR) drops, the stretch receptors in the ______________signal cells of the juxtaglomerular apparatus to secrete renin.
macula densa
The system requires pressure monitors. The kidney contains mechanisms to control blood pressure. When the glomerular filtration rate (GFR) drops, the stretch receptors in the macula densa signal cells of the _______________to secrete renin.
juxtaglomerular apparatus
JG app
The system requires pressure monitors. The kidney contains mechanisms to control blood pressure. When the glomerular filtration rate (GFR) drops, the stretch receptors in the macula densa signal cells of the juxtaglomerular apparatus to secrete ________.
RENIN
_________ is converted to angiotensin, which effects vasoconstriction, mainly in peripheral arterioles, which increases peripheral vascular resistance, thereby elevating blood pressure.
RENIN
Renin is converted to ____________which effects vasoconstriction, mainly in peripheral arterioles, which increases peripheral vascular resistance, thereby elevating blood pressure.
angiotensin
Renin is converted to angiotensin, which effects vasoconstriction, mainly in peripheral arterioles, which __________peripheral vascular resistance, thereby elevating blood pressure.
increases
Kidneys
macula densa
juxtaglomerular apparatus
RENIN
angiotensin
vasoCONSTRICTion
increase blood pressure
Kidneys
macula densa
juxtaglomerular apparatus
RENIN
angiotensin
vasoCONSTRICTion
increase blood pressure
n addition, renin stimulates release of __________ by adrenal cortical cells in the glomerulosa.
Big Al dosterone
n addition, renin stimulates release of aldosterone by adrenal cortical cells in the glomerulosa. Aldosterone exerts an effect on the ____________, causing them to increase sodium reabsorption while secreting potassium. Retention of sodium increases fluid in the vascular system to maintain pressure.
DISTAL renal tubules
n addition, renin stimulates release of aldosterone by adrenal cortical cells in the glomerulosa. Aldosterone exerts an effect on the distal renal tubules, causing them to increase sodium reabsorption while secreting potassium. Retention of sodium ___________ fluid in the vascular system to maintain pressure.
INCREASES (fluid in vascular sys to raise b.p.)
RENIN
Big Aldosterone
zona glomerulosa of adrenals
DISTAL renal tubules
Kick out K+ bums
Grab salty girls for himself (Al)
Holds salt in body to maintain b.p.
n addition, renin stimulates release of aldosterone by adrenal cortical cells in the glomerulosa. Aldosterone exerts an effect on the distal renal tubules, causing them to increase sodium reabsorption while secreting potassium. Retention of sodium increases fluid in the vascular system to maintain pressure.
Another factor in blood pressure control is _________factor released from the atria of the heart, which senses filling of blood. Increased volume, and subsequent increased filling, results in release of this factor, which inhibits sodium reabsorption at the distal renal tubule
NATRAURETIC factor from the heart to influence kidney salt reabsorption by slowing it in the distal renal tubule. Heart detects high blood pressure and wants the kidneys to drop salt into distal tubules so water will follow and b.p. will be lowered by sheer volume (urination).
What happens if the ability of the heart to control salt and water dumps by kidney is impaired?
essential hypertension

In essential hypertension the process of sodium excretion is impaired, probably due to multigenic influences
Vascular alteration: over time, hypertension results in thickening of small muscular arteries and arterioles, which makes them less responsive to _______________
vasodilators
renal artery stenosis
athersclerosis of renal artery affects RENIN levels, ergo Big Al and then blood pressure
Renal Diseases: just about any renal disease leading potentially to renal failure can result in hypertension. Such diseases can include:
*

Diabetic nephropathy
*

Glomerulonephritis
*

Renal vascular diseases (renal artery stenosis, fibromuscular dysplasia, vasculitis)
*

Dominant polycystic kidney disease
*

Renal cell carcinoma
Endocrine Diseases that lead to hypertension:
*

Cushing's syndrome with increased cortisol
*

Pheochromocytoma, with increased catecholamines (tends to be episodic)
*

Aldosterone secreting neoplasm (adrenal cortical adenoma)
Neurogenic Causes of hypertension
such as increased intracranial pressure (tends to be of sudden onset)
Vascular disease causes of hypertension:
*

Aortic coarctation
*

Vasculitis (such as polyarteritis nodosa)
*

Fibromuscular dysplasia of renal arteries
thickening of small renal arteries and arterioles over the years due to high blood pressure
nephrosclerosis

(can be benign or malignant)
hyaline arteriosclerosis
benign thickening of renal arteries and arterioles over the years due to high blood pressure

a form of nephrosclerosis
gives kidney a granular appearance`
cortical scarring due to hyaline arteriosclerosis, a benign form of nephrosclerosis
onion skin appearance of renal arteriole
concentric thickening rings due to malignant hyperplastic arteriosclerosis with malignant hypertension
what happens to the arterioles and glomeruli of diabetics
glomerular nodules (nodular glomerulosclerosis) with arteriole thickening
rare tumor of adrenal gland tissue. It results in the release of too much epinephrine and norepinephrine, hormones that control heart rate, metabolism, and blood pressure .
PHEOCHROMOCYTOMA