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187 Cards in this Set
- Front
- Back
what is autoregulation?
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If systolic stays between 60-160 ⇨ perfusion is constant
|
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If a patient has a BP <60, what could be the outcome?
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Ischemic infarct:
|
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Most common cause of bleeding into any cavity:
|
HTN
|
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If a patient has a BP >160 , what could be the outcome?
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Hemorrhagic infarct:
|
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describe the aorta: smooth muscle, compliance, type of cell, Plinear
|
thickest layer of smooth muscle
• highest compliance= Δvolumel Δpressure (due to elastin) • stratified squamous cell epithelium=> made for abrasion due to speedy RBCs • higher Plinear => blood rarely touches sides of aorta |
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why does the elderly have a wide pulse pressure
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⇧ Pressure, little ⇧ volume ⇨ thick aorta in elderly = wide pulse pressure
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treatment for wide pulse pressure in the elderly
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Tx: ⇩Cholesterol intake, Ca2+ channel blockers to control calcification
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Arteries how are they controlled?
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sympathetic control, α1 receptors
|
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Monkenberg arteriosclerosis
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old people
|
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Arteriosclerotic occlusive disease: sx and symptoms (3)
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intermitted claudication
mm. pain w/ exercise impotence |
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Hyaline arteriosclerosis
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chronic intermittent HTN
|
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Hyperplastic arteriosclerosis
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malignant HTN, capillaries ready to burst
|
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Arteriole receptors
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β2 receptors; this is why they widen when the nerve is cut
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function of the arteriole
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>>do the most to protect BP
>>most smooth muscle by cross section=> "stopcock" to control BP >>to protect the capillaries |
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what is "reactive hyperemia" of arterioles
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cut nerve=> arteriole dilation=> sympathetic control
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malignant HTN complication
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end organ damage
|
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how would a clot look like in the arteriole if
>>low BP and 1 blood supply or low BP with 2 blood supplies? |
low BP/clot => pale infarct (1 blood supply), red infarct (2 blood supplies)
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Thickest layer of SM:
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Aorta
|
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Most SM:
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Arteriole
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Largest cross-sxn area:
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Capillaries
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Highest compliance
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Aorta
|
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Capillaries describe (4)
cross sectional area wall of the capillaries filtration effect if there is a decrease in # of capillaries |
• largest cross-sectional area
• thinnest walls => diffusion • max filtration=> push nutrients out • any loss of capillaries will increase resistance |
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how are Veins and Venules controlled?
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parasympathetic control
|
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describe the veins and venules
capacitance smooth muscle valves how does blood flow |
>>most capacitance => 60% of blood is pooled here
>>least smooth muscle, 1-way valves, blood flows superficial to deep |
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how do veins work when it gets cut?
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venoconstrict (α 1 receptors) to mobilize this blood if skin gets cut (from GI, skin first)
|
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how does the vein reabsorb fluid back into the vessel
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vein ⇨ venule ⇨ higher osmolarity ⇨ suck stuff into vessel
|
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Pulse pressure
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volume rising in aorta, but blood is not flowing (Systolic -Diastolic)
Ex: Stiff aorta |
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what is Transmural pressure? at what situations is this increased?
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pressure on the sides of the vessel (⇧ collagen vascular dz)
Ptotal = PTransmural + Plinear |
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Linear pressure: what vessel is this the highest?
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1/2pv2 =pressure in the middle of the vessel (highest in the aorta)
Ptotal = PTransmural + Plinear |
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filtration forces: Hydrostatic:
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think water (⇧CHF)
|
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filtration forces Oncotic:
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think protein; mostly albumin (⇩Cirrhosis)
|
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what is flux
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Δhydrostatic-Δoncotic (capillary- interstitial)
(think of this as "transudate- exudate") |
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transudate vs. excudate: specific gravity
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Transudate: Mostly water specific gravity< 1.012
Excudate: Mostly protein (>2g/ dL): specific gravity >1.012 |
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transudate vs. excudate: LDH levels
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Transudate: Low LDH ( <200)
Excudate: High LDH (>0.6 of serum or >200) |
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trasudate causes
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Too much water:
• Heart failure • Renal failure not enough protein: • Cirrhosis (can't make protein) or (not eating protein) • Kwashiork • Menetrier's (GI losing protein) • Nephrotic syndrome (pee protein) |
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excudate causes
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Too much protein:
• Purulent (bacteria) • Hemorrhagic (trauma, cancer, PE) Fibrinous (collagen vascular dz, uremia, TB) • Granulomatous (non-bacterial) • Caseous (TB) |
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Systole
mechanism blood flow O2 krotkoff sound |
squish
⇩blood flow to coronary aa more extraction of 02 (Phase 1 Korotkoff) |
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Diastole
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filling, ⇧blood flow to coronary aa., less extraction of 02 (Phase 5 Korotkoff)
|
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Why does diastole have more blood flow?
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1) less resistance (heart relaxed, not compressing coronary vv.)
2) aortic valve closed, coronary vv. ostea are open 3) more transmural pressure in aorta |
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what is A-vo2 difference:
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>>how metabolicly active the tissue is
>>O2 went out-O2 went in came (give and take) |
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what has highest A V02 difference at rest (very high consumption)
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Heart
|
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what will have the highest A V02 after exercise
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Muscle
|
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what will have the highest AV02 after a meal
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GI
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what has the lowest A V02 all the time
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Kidney
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what will have highest AV02 after test
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Brain
|
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how does the blood flow in the body
|
SVC ⇨ RA ⇨(tricuspid)⇨ RV ⇨ (pulmonic) ⇨ PA ⇨ Lungs ⇨ PVs ⇨ LA ⇨ (mitral) ⇨ LV ⇨
(aortic) ⇨ Aorta ⇨ (Brachial Cephalic, Left Common Carotid, Left Subclavian Carotid) ⇨ rest of body |
|
what factors can Change n (viscosity) Q= ΔPr⁴/nL8π
|
⇩ via phlebotomy, ⇧via polycythemia or high glucose
Q= ΔPr⁴/nL8π |
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Change L Length of vv: Q= ΔPr⁴/nL8π
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⇧via obesity
|
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how can one change the r (radius) in the poissel's law equation
Q= ΔPr⁴/nL8π |
⇩via atherosclerosis
|
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describe resistance in series?
what happens to flow and velocity as resistance increases? |
As resistance increases, flow decreases and velocity increases
o Ex: squeezing a garden hose |
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2 organs that have resistance in series
|
higher pressure
o Liver - detoxification (portal ⇨ hepatic vein) Slow stuff down to detoxify, then shoot it out ... Macrophage "security men" need to find the junk o Kidney- filtration (afferent ⇨efferent arteriole) Blood is sitting in "traffic jam" |
|
Resistance in parallel:
what organs have this? what happens to resistance when organ is removed what happens during pregnancy? after labor? predict the BP? |
most of our organs have this 1/Rtotal= 1/R1+1/R2 ect.
Ex: Remove an organ=> increase resistance (transient ⇧BP) Ex: Add a baby=> decrease resistance (why BP is low in pregnancy) |
|
Vasodilators:Brain:
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⇧pco2, ⇩po2
Ex: High altitude: low p02 => hyperventilation (chronic=> pulm vasoconstrict, secrete bicarb) |
|
Vasodilators: Heart:
|
Adenosine
Ex: ⇧flow to SA node to prevent ischemia ⇨stop arrhythmia ⇨pause (Na channels reset) ⇨restart heart |
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Vasodilators: Lungs
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⇧po2
Ex: hypoxia vasoconstricts blood vessels to lungs = > polycythemia |
|
Vasodilators: kidneys
|
Kidney: PG-E, DA, ANP
Ex: DA used in shock to increase blood flow to the kidneys Ex: NSAIDs will decrease blood flow to kidney => bad for elderly |
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Vasodilators:GI:
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Food
Ex: blood rushes to stomach after meal |
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what factors would vasodilate the Skin:
|
Temp, ⇧pC02
Ex: Face flushes in hot summer (builds up w/ walking, need blood flow to wash it out) |
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Vasodilators:Muscle:
|
⇩pH, ⇧pC02
Ex: Exercise |
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when you stand up what happens normally to heart rate and BP?
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when you stand up: BP ⇩5-10mm Hg and ⇧Pulse 10-15 bpm
|
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if after standing up pulse goes up >10 dx.
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If pulse goes up >10 =>hypovolemia
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Early Shock: what happens to pulse and diagnosis.
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CO = HR(pulse) x SV (blood pressure)
PULSE ⇧>10 when stand (orthostatic hypotension = compensated shock) |
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Late Shock: what happens to BP and diagnosis
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CO = HR(pulse) x SV (blood pressure)
BP⇩ >10 when stand (uncompensated=> low CO) |
|
when a person stands up from a sitting
position and the pulse goes up <5 what does it lead to? |
=> Autonomic Dysfunction: stand up and pass out w/o warning
|
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most common cause of autonomic dysfunction in Adults:
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DM (infarcts carotid sinus)
|
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most common cause of autonomic dysfunction in Elderly: and tx
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Sick Sinus syndrome (Tx: Pacemaker)
|
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most common cause of autonomic dysfunction in Parkinson's:
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Shy-Dragger syndrome
|
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most common cause of autonomic dysfunction in Babies:
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Riley-Day "Familial Dysautonomia" (no reflexes)
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Carotid Body:
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Chemoreceptor
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Carotid Sinus:
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Baroreceptor
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how does your body respond to Low volume State immediately?
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Carotid sinus baroreceptor- ⇧sympathetics => high HR (reflex tachycardia)
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how does your body respond to Low volume State Intermediate?
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Medulla- releases NE => vasoconstrict = >high HR and TPR
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how does your body respond to Low volume State Long-term?
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Kidneys - release renin => high TPR, ⇧Na resorption and ⇧K excretion. Excess water
reabsorption leads to dilutional ⇩Na,⇩Cl, ⇩K. ⇧K excretion leads to alkalosis. |
|
Carotid sinus immediate response to low volume state
sv ~>stretch~> carotid sinus~>CN9 (aff) ~>CN10 (eff) ~>sympathetics ~>HR,BP |
⇩sv ~>⇩stretch~> carotid sinus~> -⇩-CN9 (aff) ~> -⇩-CN10 (eff) ~> ⇧sympathetics ~> ⇧HR, ⇧BP
|
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how does the carotid sinus regulate BP?
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baroreceptor that responds to stretch (volume) => regulate BP
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how can we Increase SV?
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• Rub carotid sinus
• Vasovagal response (cough, sneeze, urinate) ~> replicate with tilt test |
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how can we Decrease SV? (3)
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• Tonsillectomy (cut CN9) don't do it before 2 years old
• Stand up (blood drained down) • Nitrates for angina (so ... give β blocker first for MI pts to protect heart) |
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Medulla's intermediate response: on low volume state
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The nucleus tractus solitarius ~> NE release (higher affinity for α receptors) ~> constrict~> increase HR and TPR (reflex tachycardia)
|
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Kidney's long-term (>20 min) response: after the medulla releases NE on low volume state
|
• NE also vasocontricts blood supply to kidney
• J -G apparatus in afferent arteriole of the kidney responds to flow and volume |
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How does our body Fix the Pressure:
|
Mr. J-G releases renin~> Liver (angiotensinogen) ~> ATI ~>Lungs (ACE) ~>
ATII (very potent vasoconstrictor) to efferent arteriole -> ⇧TPR ~> ⇧BP ATII constricts efferent more than afferent in order to re-establish GFR |
|
how does our body Fix the volume?
|
ATII ~> Aldo ~> Na + /K pumps in kidney DCT ~> ⇧Na reabsorption ~> ⇧total body water ~> drags in 3
waters with each Na ~> decreases serum Na ~> serum K decreases (secretion) ~> Aldo also secretes H+ ~> ⇧pH |
|
Vomiting: alkalosis/acidosis
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Alkalosis
|
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Diarrhea: alkalosis/acidosis
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Acidosis
|
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Low Volume state normally cause alkalosis, what Low volume state causes acidosis (what are the exceptions)?
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Acidosis Exceptions:
• Diarrhea (lose bicarb) => acidosis • RTA type II (lose bicarb) =>acidosis • DKA (ketones) = > acidosis |
|
what are the High Na Exceptions:
|
• Diabetes Insipidus
• Neglected elderly (eating salt, but not drinking pure water) |
|
What is the Physiology of a Man in the Desert? Effect of Low Volume on Heart: Fluid volume~>Preload~> RA filling~>RV filling~>Ventricular contractility~>Softer S1 (pressure)~>Narrow S2 splitting (volume/ pressure)~>CVP~>EKG amplitude~>Vascular pressure ~>Pulmonary resistance~>PCW~>LV filling~>Contractility of heart ~>Stroke volume~>Cardiac output~>Blood flow~>Carotid stretch~>Firing of CN 9/10~> Heart rate
|
decrease in everything except HR which is increased)
Fluid volume~>Preload~> RA filling~>RV filling~>Ventricular contractility~>Softer S1 (⇩pressure)~>Narrow S2 splitting (⇩volume/ ⇩pressure)~>CVP~>EKG amplitude~>Vascular pressure ~>Pulmonary resistance~>PCW~>LV filling~>Contractility of heart ~>Stroke volume~>Cardiac output~>Blood flow~>Carotid stretch~>Firing of CN 9/10~>⇧ Heart rate |
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Physiology of a Man in the Desert? Effect of Low Volume on Kidneys:Firing of CN 9/10~>NE release~>TPR~>Blood flow sensed by J-G apparatus~>Renin release~>Angiotensinogen in liver~>Angiotensin I in lung~>Angiotensin II (coverted by ACE in lung)~>Vasoconstriction~>TPR more~>Aldosterone in the CD~>Na/H20 reabsorption~>K/H
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⇩Firing of CN 9/10~>⇩NE release~>⇧TPR~>⇩Blood flow sensed by J-G apparatus~>⇧Renin release~>⇧Angiotensinogen in liver~>⇧Angiotensin I in lung~>⇧Angiotensin II (coverted by ACE in lung)~>⇧Vasoconstriction~>⇧TPRmore~>⇧Aldosterone in the CD~>⇧Na/H20 reabsorption~>⇩K/H
|
|
Effect of Low Volume on Urine:
?urine Na (?Na/H20 reabsorption)~>?urine K~>?urine pH (?urine H+)~>?FeNa |
Effect of Low Volume on Urine:
⇩urine Na (⇧Na/H20 reabsorption)~>⇧urine K~>⇧urine pH (⇩urine H+)~>⇧FeNa |
|
Effect of Low Volume on Serum:
Total body Na (Na reabsorption by Aldo)~>serum Na (H20 reabsorption by Aldo)~>1 serum K ( K excreted by Aldo)~>serum pH (H+ excreted by Aldo) |
⇧Total body Na (⇧Na reabsorption by Aldo)~>⇩serum Na (H20 reabsorption by Aldo)~>⇩ serum K ( K excreted by Aldo)~>⇧serum pH (H+ excreted by Aldo)
|
|
Effect on Low Volume on Lung:
serum pH~>Harder to breathe in~>Restrictive lung disease~>p02 (hard to breathe in)~>Respiratory rate~>C02~>serum pH~>Respiratory alkalosis |
⇧serum pH~>Harder to breathe in~>Restrictive lung disease~>⇩p02 (hard to breathe in)~>⇧Respiratory rate~>⇩C02~>⇧serum pH~>Respiratory alkalosis
|
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Only Veins with No Valves:
|
• Brain
• Heart |
|
Superficial Vein Thrombosis: describe and tx
|
• Red cord
• Varicose veins • Tx: warm compresses |
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Low Risk DVT: what is the DVT prophylaxis
|
SCDs
|
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Moderate Risk DVT: what is the DVT prophylaxis
|
Heparin
|
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DVT Prophylaxis High Risk
|
(Ortho/Neurosurgeons/Previous DVT): warfarin with INR of 2-3
|
|
DVT Tx:
|
LMW Heparin+ Warfarin (can tx outpatient if no pulmonary sx or co-morbidities)
|
|
Thrombus:
|
artery occlusion
|
|
Emboli
|
moving thrombus
|
|
IgA Deficiencies:
|
• Giardia
• Ataxia Telangiectasia |
|
bugs that have IgA Proteases:
|
• Strep pneumo
• H. influenza • N. catarrhalis |
|
diseases with IgA Nephropathies (4)
|
• Alport's
• HSP • Berger's • Ankylosing Spondylitis |
|
Rathke's Pouch =>
|
• Anterior pituitary
• Hard palate |
|
CVAs:
what is a Stroke: |
infarcted cerebral tissue
|
|
CVAs:TIA:
|
neurologic deficits < 1hr w / no infarction
|
|
Dx: CVA (2) and medical therapies (3)
|
US ⇨ carotid stenosis
TEE ⇨ embolus • Antiplatelets (asa, Clopidogrel) • Anticoagulate (Heparin, warfarin) • Thrombolytics (t-PA) |
|
DDX:/Sx Strokes at Carotid: anterior circulation (4)
|
• TIA
• Amaurosis Fugax • Aphasia • Clumsy hands |
|
Strokes at the Vertebrobasilar: posterior circulation
|
SAND
• N/V • Syncope • Ataxia • Diplopia |
|
Stroke Management:
|
1) CT: rule out hemorrhagic stroke
2) Treat based on time symptoms began: • <3hr: t-PA (IV) • 3-6 hr: t-PA (intra -arterial) • 7-8 hr: Embolectomy • 9+hr: Dipyridamole+ asa |
|
Agnosia:
|
difficulty with comprehension
|
|
Agoraphobia:
|
fear of not being able to escape "can't go"
|
|
Anosagnosia:
|
can't understand that they are sick
|
|
Apraxia:
|
can't follow commands
|
|
Aphasia:
|
can't speak due to brain problem
|
|
Dysarthria
|
can't speak due to muscle problem
|
|
Agraphia:
|
can't write
|
|
Anomia
|
can't remember names
|
|
Prosopagnosia
|
can't remember faces
|
|
what would the CBC of every vasculitis would look like?
|
⇩RBC, ⇩platelets, ⇧WBC, ⇧T cells, ⇧MP, and schistocytes
|
|
for collagen vascular disease what would be up as well
|
eosinophil count will also be elevated.
CBC:⇩RBC, ⇩platelets, ⇧WBC, ⇧T cells, ⇧MP, and schistocytes |
|
tie in the vasculitis into concept into LES
|
You have a vasculitis, and your RBC count is low. What do you need RBC for?
oxygen. And what do you need oxygen for? Making energy. So what state are we in? The low energy state. |
|
what would be seen in vasculities
|
• Low volume state, low energy state, restrictive lung dz profile, cell-med inflammation
• Exposes BM~>shows GP2b3a, which attracts platelets • ⇩RBC/platelets, ⇧WBC/T cells/ MP, schistocytes |
|
Ankylosing Spondylitis
pt complaint x-ray test HLA association inheritance |
Middle-age male w / back pain, bamboo spine, + Schober test, HLA-B27, AR
|
|
Alport's
|
IgA deposition, deaf or cataract family
|
|
Behset's
|
RA + oral and genital ulcers
|
|
Berger's
|
IgA deposition 2 wk after cold ~> renal failure (hematuria, edema)
|
|
Buerger's
|
Smoking Jews, necrosis of extremities
|
|
Churg-Strauss: associated problems, antibody, unique features
|
Pulmonary eosinophils, asthma, p-ANCA
|
|
CREST: syndrome of what kind of scleroderma and its antibody
|
syndrome Mild scleroderma, anti-centromere Ab
|
|
Cryoglobulinemia: what kind of inflammation and Ig
|
Acute non-bact inflammation ( < 2mo ), IgM
|
|
Diabetes mellitus: neuropathy distribution
|
Glove-and-stocking distribution
|
|
Disseminated Intravascular Coagulation "DIC": causes (3) and what would be seen.
|
Sepsis, amniotic fluid emboli, abruptio placenta, D- dimers = fibrin split products
|
|
Felty's
|
RA + leukopenia + splenomegaly
|
|
Goopasture's Lung and kidney
Ab and what would be seen on BM |
anti-GBM Ab, linear BM
in imunofluorescence |
|
Hemolytic Uremic Syndrome
|
"HUS" Child renal failure 2 wk after eating raw hamburgers
|
|
Henoch-Schonlein Purpura "HSP"
onset and Ig associated syndrome platelet levels presentation of rash Tx |
down "Hip-South Purpura
"IgA deposition 2 wk after gastroenteritis, intussusception, normal Plt, purpuric rash from butt T x: Steroizds/ Immunosuppresants |
|
Immune Thrombocytopenic Purpura:
onset and Ab |
Purpura 2wk after URI, anti-platelet Ab
|
|
Immune Thrombocytopenic Purpura: tx
|
Tx:
1) Prednisone 2) IVIg 3) Splenectomy |
|
Kawasaki Disease: presentation
|
"CRASH"
Strawberry tongue, red eyes/lips, palm/sole rash, cervical lymph nodes, kid MIs, high platelets, fever, |
|
Kawasaki Disease: tx
|
Tx: ASA + flu shot, IVIg
|
|
Leukocytoclastic Vasculitis
|
Drug allergy causes vasculitis
|
|
Mixed Connective Tissue Disease ab
|
Anti-RNP Ab
|
|
MPGN type l
|
C3 nephritic factor
|
|
MPGN type II
|
Kidney deposits, tram-tracks, low C3
|
|
Polyarteritis Nodosa "PAN"
attacks what organs antibody associated disease apprerance |
GI and kidney, P-ANCA Ab, HepB, mottled lace-like
appearance |
|
Polyarteritis Nodosa "PAN" Test:
|
Biopsy or Visceral Angiography
|
|
Post-strep Glomerulonephritis
onset deposits strain |
2 wk after sore throat, Subepithelial deposit
strain 12 |
|
Progressive Systemic Sclerosis
|
Scleroderma that attacks organs~
|
|
Rheumatoid Arthritis
presentation pathogenesis of pannus and cardia antibody joints involved in the head |
Worse in morning, attacks synovium => pannus,
amyloid =>restrictive cardia, RF, attacks C1-C2 joint |
|
scleroderma: ab
|
Anti-Scl70 Ab
|
|
Serum sickness
|
2 wk after vaccination (MMR)
|
|
Sjogren's
presentation (3) antibody |
RA + sica (xerostomia/xeropthalmia), anti-SSB Ab,
dental cavities |
|
Still's disease= Juvenile RA
|
Iridocyclitis + RA
|
|
Subacute Bacterial Endocarditis
most common cause |
Septic emboli, Strep viridans
|
|
Temporal Arteritis
presentation ESR levels |
Unilateral temporal HA, jaw claudication, ESR >60
|
|
Syphilis
|
Aortitis, wriinkled intima, tree-bark appearance, obliterative endarteritis
|
|
Systemic Lupus Erythematosis "Lupus"
antibody MCC of death deposits (Ig) complement rash |
Ab: dsDNA/Sm/ Cardiolipin, malar rash, die of renal
failure, subepithelia/ deposit, IgG at derm-epid jxn, granular complement |
|
Systemic Lupus Erythematosis
"Lupus" TX |
Tx: NSAIDs. Cyclophosphamide,
hydroxychloroquine |
|
Takayasu's = "aortic arch syndrome" (4)
|
Weak pulse, aortitis, Asian women, blind, Raynaud's,
acute pain with cold |
|
Takayasu's = "aortic arch syndrome" tx
|
Tx: daily high-dose steroids
|
|
Thrombotic Thrombocytopenic Purpura "TTP"
presentation deficiency and tx |
Purpura + neuro symptoms, VWF esterase deficiency
Tx: Plasmapheresis |
|
Trousseau's
|
Migratory thrombophlebitis, assoc w / cancer
|
|
Wegener's "whole lot of crap"
attacks what organs ab |
Lung, kidney, and sinus, c-ANCA Ab
|
|
Palm/Sole Rashes:
|
''TRiCKSSS''
Toxic Shock Syndrome Rocky mountain spotted fever Coxsackie A: Hand-Foot-Mouth disease Kawasaki Scarlet fever Staph Scaled Skin Syphilis |
|
High platelet count
|
Kawasaki
|
|
Normal platelet count:
|
HSP
|
|
ABI:
1.0: <0.9: <0.4: |
ABI:
1.0: Normal <0.9: PVD <0.4: Severe ischemia |
|
what are HLA-B27 Diseases:
|
• Psoriatic Arthritis
• Ankylosing Spondylitis • Reiter's |
|
Psoriatic Arthritis:
involves what joints bones, nails and extensors stones and associated syndrome |
attacks DIP joints, silver oval plaques on extensors, nail pitting, pencil-thin bones, gout, uric acid kidney stones
|
|
Ankylosing Spondylitis
Inheritance: presentation pathogenesis x-ray test |
inheritance: AR
pathogenesis: Ligament ossification, presentation: uveitis, decreased Lumbar curve, stiffer in morning, kyphosis, x-ray: bamboo spine, test: (+) Schober test |
|
Reiter's
|
Uveitis, Urethritis, Arthritis
|
|
what are the Pulmonary Eosinophilias:
|
• Aspergillus (Tx: Steroids)
• Loeffler's (Tx: Antibiotic or Anti-parasitic) • Churg-Strauss (Tx: Zafirlukast) |
|
Aspergillus tx
|
Tx: Steroids
|
|
Loeffler's tx
|
Tx: Antibiotic or Anti-parasitic
|
|
Churg-Strauss tx
|
Tx: Zafirlukast
|
|
Low C3 diseases
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"PMS in Salt Ltke City"*
Post-strep GN MPGN Type II Subacute Bacterial Endocarditis Serum sickness Lupus Cryoglobulinemia |
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CREST:
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Calcinosis
Raynaud's Esophageal dysmotility Sclerodactyly Telangiectasia |
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Bacterial Endocarditis: tx
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Bacterial Endocarditis: (Tx: Nafcillin + Gentamycin)
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Bacterial Endocarditis: acute vs subacute
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Acute: Staph Aureus => attacks healthy valves
Subacute: Strep viridans => attacks damaged valves |
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bacterial Endocarditis Dx:
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TEE
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bacterial Endocarditis Septic emboli can lead to what complication?
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ischemic stroke
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bacterial endocarditis: septic emboli in the Brain
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Mycotic aneurysm
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bacterial endocarditis: septic emboli in the Retina (describe)
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Roth spots (central white hemorrhagic spots)
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bacterial endocarditis: septic emboli in the Fingers/Toes:
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Osler nodes (painful red nodules) "ouch"
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bacterial endocarditis: septic emboli in the Nailbed:
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Splinter hemorrhage
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bacterial endocarditis: septic emboli in the Palm/Soles
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Janeway lesions (painless dark macules)
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Cryoglobulinemia: pathogenesis
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serum proteins (i.e. globulins) form a gel when exposed to cold
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bugs that cause Cryoglobulinemia:
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"I AM HE"
Influenza Adenovirus Mycoplasma Hep B/C EBV |