Pathophysiology 4 - Cardiovascular system
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
Help!
|
|
||||
|---|---|---|---|---|---|
| what is blood | connective tissue that circulates the body
🗑
|
||||
| what are the three functions of blood | - transport
- protection
- regulation
🗑
|
||||
| what does the blood transport | - gases
- nutrients
- wastes
- hormones
🗑
|
||||
| what does the blood regulate | - temperature
- pH
- fluid volume
🗑
|
||||
| how does the blood protect | - protects against blood loss
- protects against infection
🗑
|
||||
| there are two components of blood | plasma (liquid components) and formed elements (solid components)
🗑
|
||||
| what are the formed elements of blood | - red blood cells (erythrocytes)
- white blood cells (leukocytes)
- platelets
🗑
|
||||
| majority of plasma proteins are | albumin
🗑
|
||||
| name the plasma proteins | - albumin
- globulins
- fibrinogen
🗑
|
||||
| describe erythrocytes | - transport gases
- biconcave discs
- anucleic
- no organelles
- have hemoglobin
- synthesized in bone marrow
🗑
|
||||
| what are the function of platelets | - assists in blood clotting
- releases chemical messengers
🗑
|
||||
| what is homeostasis | - the stoppage of blood flow
🗑
|
||||
| list the three stages of homeostasis | 1) vascular constriction
2) formation of the platelet plug
3) Blood coagulation
🗑
|
||||
| function of aspirin/clopidogrel | - platelet aggregation inhibitors
- prevent clot formation
🗑
|
||||
| list three diseases that ASA and Plavix help treat | - Peripheral artery disease
- strokes
- myocardial infarctions
🗑
|
||||
| a primary blood disorder | the problem starts within the blood
🗑
|
||||
| a secondary blood disorders | the cause agent is not with the blood
🗑
|
||||
| describe qualitative | cell abnormalities of plasma factor dysfunction
🗑
|
||||
| describe quantitative | increase/decreased cell production/destruction
🗑
|
||||
| define anemia | when there is a decrease in oxygen carrying capacity resulting in decreased oxygen to body tissue. it can be from insufficient erythrocytes of decreased hemoglobin
🗑
|
||||
| etiology/mechanisms of anemia | - blood loss
- decreased RBC production
- increased RBC destruction
- deficiency anemias
🗑
|
||||
| (name at lease 5) clinical manifestations of anemia | - tiredness
- weakness
- pale skin
- rapid/irregular heart beat
- dyspnea
- dizziness
- lightheadedness
- headaches
- chest pain
- cold hands/feet
🗑
|
||||
| causes of acute anemia | - surgery
- cuts
- trauma
🗑
|
||||
| causes of chronic anemia | - internal bleeding (ulcer)
- menstrual issues
- chronic infection (AIDS, Cancer, Autoimmune)
- inflammation
🗑
|
||||
| cause of aplastic anemia | ~ 50% is idiopathic
-when bone marrow fails to produce RBCs
🗑
|
||||
| labs that would help identify chronic anemia | - mild anemia
- high ferritin
- low reticulocytes
- low TIBC
- low transferrin
🗑
|
||||
| list a couple causes of hemolytic anemia | - infections
- drugs
- cancers
- autoimmune
🗑
|
||||
| define normochromatic | normal color of RBCs
🗑
|
||||
| define hypochromatic | decreased color of RBCs
🗑
|
||||
| define normocytic | normal RBC size
🗑
|
||||
| define microcytic | small RBC size
🗑
|
||||
| define macrocytic | large RBC size
🗑
|
||||
| why is RBC size and shape important | it gives us information about cause of anemia
🗑
|
||||
| what is transferrin | - transports iron in blood
- measured with Total Iron Binding Capacity (TIBC)
🗑
|
||||
| TIBC | Total Iron Binding Capacity
🗑
|
||||
| etiology of sickle cell anemia | - point mutation (recessive trait)
- causes abnormal Hemoglobin S (HbS)
🗑
|
||||
| heterozygous sickle cell | sickle cell trait
🗑
|
||||
| homozygous sickle cell | sickle cell disease
🗑
|
||||
| mechanism of sickle cell anemia | - cells become sickled with deoxygenation
- increases RBC adhesiveness and adherence
🗑
|
||||
| clinical manifestations of sickle cell anemia | - blood vessel occlusion
- ulcer formation (due to lack of blood flow and ischemia)
- **acute chest syndrome**
- functional asplenia
- hyperbilirubinemia (causing jaundice and gall stones)
🗑
|
||||
| the leading cause of hospitalization for those with sickle cell anemia | acute chest syndrome
🗑
|
||||
| symptoms and other clinical presentations related to acute chest syndrome | - atypical pneumonia
- pulmonary infarction
- dyspnea
- chest pain
- cough
🗑
|
||||
| how is sickle cell anemia diagnosed | - hemoglobin electrophoresis
- all other hemoglobinopathies are done at birth
🗑
|
||||
| treatment for sickle cell anemia | - no known treatment
- focused on preventing sickling episodes
- goal is symptom management
🗑
|
||||
| describe the treatment for sickle cell symptoms | - immunization is key
- hydroxyurea (medication) to promote synthesis of more HbF and less HbS
🗑
|
||||
| etiology for Thalassemia | - inherited
- two types
------ alpha Thalassemia (mostly Asian)
------ beta Thalassemia (mostly Mediterranean European)
🗑
|
||||
| what is Beta Thalassemia | the deficiency is in the Beta chain
🗑
|
||||
| what is Alpha Thalassemia | the deficiency is in the alpha chain
🗑
|
||||
| heterozygous thalassemia | thalassemia minor
---- normal hemoglobin synthesis
---- prevents severe anemia
🗑
|
||||
| the mechanisms of thalassemia | - increase in erythropoietin secretion
- hypochromic and microcytic anemia
- decreased synthesis of affected chain
- accumulation of affected globulin chain
🗑
|
||||
| clinical manifestations of thalassemia | - severe growth retardation (if left untreated)
- hyperplasia of bone marrow (impairs bone growth)
- splenomegaly
- osteoporosis
- osteopenia
- hepatomegaly
🗑
|
||||
| treatment(s) of thalassemia | - blood transfusions early in life and regularly throughout life (iron overload is a complication of this)
- iron chelation therapy (reduces iron overload)
🗑
|
||||
| how do you treat chronic inflammation anemia | - underlying disease
- erythropoietin therapy
- iron supplements
- blood transfusions
🗑
|
||||
| etiology/mechanisms of iron deficiency anemia | - loss of iron (through bleeding, chronic or acute, most common cause world wide)
- increased demand (pregnancy)
- iron deficient diets
- chronic blood loss (most common in developed world)
🗑
|
||||
| chronic blood loss is the most common cause of iron deficiency anemia in the developed world. list at lease 3 causes of this type of anemia | - menses
- GI bleed
- hemorrhoids
- vascular lesion
- intestinal polyps
- cancer
🗑
|
||||
| clinical manifestations of iron deficiency anemia | - impaired oxygen transport
- fatigue
- palpitations
- angina
- tachycardia
- brittle hair/nails
- sores in mouth
- pica (ice/dirt)
🗑
|
||||
| how to diagnose iron deficiency anemia | - (on CBC) decrease in hemoglobin
- (on CBC) decrease in Hematocrit
- decrease in iron stores/serum iron/(most specifically) ferrin levels
- increase in total iron binding capacity (TIBC)
🗑
|
||||
| treatment for iron deficiency anemia | - prevention is key
- 0-1 year old
---- avoid cows milk
---- iron fortified diet
- 1(+) years
----- iron rich foods and supplements
----- treating chronic blood loss
🗑
|
||||
| metablastic anemias | vitamin B12 and folic acid deficiencies
🗑
|
||||
| etiology of B12 deficiency | - B12 and folic acid deficiency (slowly develops, dietary deficiency is rare)
- lack of interinsic factor (possibly autoimmune, neoplasms, gastrectomy/ileal resection)
🗑
|
||||
| what is pernicous anemia | anemia caused by lack of intrinsic factor (produced in stomach)
🗑
|
||||
| what is the mechanism for B12/folic acid anemia | enlarged RBCs (megaloblastic anemia)
🗑
|
||||
| what are some clinical presentations of b12/folic acid anemia | - moderate-severe anemia
- mild jaundice
- neurological changes (like peripheral neuropathy, confusion, dementia)
- myelin breakdown
🗑
|
||||
| how is b12/folic acid anemia diagnosed | - elevated MCV, yet normal MCHC
- low serum B12
- schillint test mesure
🗑
|
||||
| treatment for B12 anemia | - B12 injections for life
- high doses orally
🗑
|
||||
| why is folic acid important for life | required for DNA and RBC maturation
🗑
|
||||
| how can folic acid be obtained | - found in vegetables, fruit, cereal, meat
- absorbed in the intestine
- also lost in cooking
🗑
|
||||
| what is the most common cause of folic acid anemia | - malnutrition
- mediation and tumor cells can also block folic acid absorbtion
🗑
|
||||
| agranulocytosis is the same term as | neutropenia
🗑
|
||||
| what is neutropenia | - lack of wbc
- puts a person at risk for infection
🗑
|
||||
| etiology of neutropenia | - bone marrow failure
- infection/sepsis
- medications (chemotherapy)
- abscesses
🗑
|
||||
| list some signs and symptoms of neutropenia | - infections
- malaise
- chills
- fever
- weakness
-fatigue
🗑
|
||||
| what is homeostasis | arrest of bleeding
🗑
|
||||
| 5 steps of homeostasis | 1) vascular spasm (constriction)
2) formation of platelet plug
3) coagulation (clotting)
4) clot retraction
5) clot dissolution
🗑
|
||||
| what is a thrombus (the most common type of thrombus) | a clot that develops and persists in unbroken vessel (DVT)
🗑
|
||||
| what is an embolus (the most common types) | -thrombus freely floating in blood stream
(pulmonary embolus, cerebral embolism)
🗑
|
||||
| thrombocytosis | increased platelet
🗑
|
||||
| arterial thrombus is associated with atherosclerosis and results from ___________________ | - increased platelet number or restricted blood flow with platelet adhesion
🗑
|
||||
| causes of secondary hypercoagulability states | - increased pro-coagulation factors (increased platelet activity)
- decreased anticoagulation factors (conditions that cause increased activity of coagulation pathways)
🗑
|
||||
| list some causes of bleeding disorders | - platelet coagulation factors
- blood vessel structure
🗑
|
||||
| list three types of thrombocytopenia | - drug-induced thrombocytopenia (DITP)
- Heparin Induced Thrombocytopenia (HIT)
- Immune Thrombocytopenic Purpura (ITP)
🗑
|
||||
| DIC stands for | Disseminated Intravascular Coagulation
🗑
|
||||
| what is DIC | -clots form and simultaneously hemorrhage at the same time
🗑
|
||||
| etiology of Hemophilia | - X-linked recessive trait
- leads to defective clotting factors.
🗑
|
||||
| clinical presentations of hemophilia | - spontaneous and prolonged bleeding
- hematuria
- epistaxis
- hemarthrosis
🗑
|
||||
| how is hemophilia treated | - replacing clotting factors
- use of drugs to proliferate vW factor or antifibgolytic
🗑
|
||||
| risk factors for secondary hypercoagulation (atherosclerotic plaque) | - increased cholesterol levels
- diabetes
- smoking
🗑
|
||||
| two major characteristics of thrombocytosis | - platelet count > 450k/microL
- regulated by a *negative* feedback loop
🗑
|
||||
| what is erythromelalgia | painful throbbing in fingers caused by occlusion in arterioles
🗑
|
||||
| secondary thrombocytosis usually occurs because of | a diseased state
🗑
|
||||
| primary hypercoagulability condition is caused by | - it is inherited
- factor V gene (prothrombin gene/factor V Leiden mutation) is the most common
🗑
|
||||
| the mechanism of the factor V gene in a primary hypercoagulability state | it cannot be activated by protein C
🗑
|
||||
| what is antiphospholipid syndrome | autoantibodies (mostly IgG) acting against protein -binding phospholipids
🗑
|
||||
| what are the clinical manifestations of the antiphospholipid syndrome | - arterial thrombin
- recurrent miscarriages
- thrombocytopenia
🗑
|
||||
| Hemophilia A | - factor VIII deficiency
- X-linked recessive disorder
- while it does run in families it can be spontaneous.
🗑
|
||||
| Hemophilia B | - factor IX deficiency
🗑
|
||||
| 4 parameters of Cardiac Function | - contractility
- preload
- After load
- heart rate
🗑
|
||||
| what is contractility | the ability of a heart to change rate of force of contraction without a change in diastolic length
🗑
|
||||
| what do positive intropic effects do | increase heart contractile force
🗑
|
||||
| list some things that have a positive intropic effect on the heart (name 3) | - Sympthaetic Nervouse system
- afterload
- catecholamines
- increased heart rate
- drugs
- intracellular calcium levels
🗑
|
||||
| what do negative intropic effects do | decrease contractility
🗑
|
||||
| list 4 things that have a negative intropic effect on the heart | - parasympathetic nervous system
- heart failure
- hypoxia
- drugs
🗑
|
||||
| what is the frank-starling principle | as end diastolic volume increases then the force of contraction also increases
🗑
|
||||
| the frank-starling principle fits into which parameter of cardiac function | preload
🗑
|
||||
| what is preload | the amount of blood volume has to pump with each beat
🗑
|
||||
| larger preload means | a higher end diastolic volume
🗑
|
||||
| two major factors effecting preload | - venous return
- filling time
🗑
|
||||
| venous return is affected by | - blood volume
- muscular activity and rate
🗑
|
||||
| filling time is affected by | heart rate
🗑
|
||||
| what is afterload | - the pressure in the aorta that the ventricles must overcome to eject blood
🗑
|
||||
| what increases afterload | any factor that restricts blood flow through the arterial system
-- vasoconstriction
-- hypertension
🗑
|
||||
| what decreases afterload | vasodilation
🗑
|
||||
| an increased afterload also increases what | end systolic volume
🗑
|
||||
| what is ESV | end systolic volume (blood left in ventricles after systole)
🗑
|
||||
| ejection fraction | end diastolic volume/end systolic volume (should be around 60%)
🗑
|
||||
| average cardiac output (what is the number and unit) | 4-6 L/minute
🗑
|
||||
| what does cardiac output measure | volume of blood pumped out of heart per minute
🗑
|
||||
| how is cardiac output measured | stroke volume (SV) X heart rate (HR)
🗑
|
||||
| what is stroke volume | the volume of blood expelled by ventricles with each beat
🗑
|
||||
| how is stroke volume measured | end diastolic volume - end systolic volume
🗑
|
||||
| what is pericardium | though, thick sac surrounding the heart
🗑
|
||||
| what is the purpose of the pericardium | - holds heart in place
- acts as a barrier to infection
🗑
|
||||
| what is the septum | the wall that separates the chambers of the heart into right side and left side
🗑
|
||||
| mitral valve is located | between left atrium and left ventricle
🗑
|
||||
| mitral valve is also called | bicuspid valve
🗑
|
||||
| where is the tricuspid valve located | right side (between atrium and ventricle)
🗑
|
||||
| route of the electrical signal that creates a heart beat | - Sinoatrial (SA) node
- atrioventricular (AV) node
- Bundle of His
- Perkinje fibers
🗑
|
||||
| what is cardiac reserves | max % of cardiac output that can be achieved above normal resting level (300-400%)
🗑
|
||||
| what is ejection fraction | the amount of blood pumped out of the heart with head ventricular contraction
🗑
|
||||
| what are the two parts of the circulatory system | - pulmonary circulation
- systemic circulation
🗑
|
||||
| what are hemodynamics | principles that regulate blood flow
🗑
|
||||
| what are the three factors of hemodynamics | - pressure
- resistance (opposition to blood flow)
- flow
🗑
|
||||
| two factors that affect blood flow | - radius of the blood vessel
- blood viscosity (fluid thickness)
🗑
|
||||
| define compliance | - total quantity of blood that can be stored in a given portion of the circulation for each millimeter of mercury (mmHg) rise in pressure
🗑
|
||||
| the mathematical relationship between compliance and volume and pressure | - there is a direct relationship between an increase volume and compliance
- there is an indirect relationship between increased pressure and compliance
🗑
|
||||
| what is compliance REALLY measuring | - the ability of a vessel to distend and increase volume with increasing pressure
🗑
|
||||
| (arteries/veins) are most compliant vessels | veins (they can handle increased volume with minor pressure changes)
🗑
|
||||
| what is wall tension | the force in the vessel wall that opposes the distending pressure inside the vessel
🗑
|
||||
| why is blood pressure important | it helps keep a constant flow to the body's vital organs
🗑
|
||||
| why is hypotension dangerous | it can prevent adequate blood flow to tissue and other organs
🗑
|
||||
| why is hypertension dangerous | it can be fatal
🗑
|
||||
| what is pulse pressure | the difference between SBP and DBP
🗑
|
||||
| what is typical pulse pressure | 40 mmHg
🗑
|
||||
| what are the two factors that affect blood pressure | - stroke volume
- total distensibility of the atrial tree
🗑
|
||||
| what is mean atrial pressure | - average pressure in the arterial system during a cardiac cycle (~90-100 mmHg)
🗑
|
||||
| mean atrial pressure is a good indicator of | tissue perfusion
🗑
|
||||
| how is mean arterial pressure measured | cardiac output (HR x SV) x Perpheral vascular resistance (PVR)
🗑
|
||||
| neural mechanisms for BP control | autonomic nervous system and barioreceptors (found in the walls of the great vessels and heart, pressure sensitive)
🗑
|
||||
| list three humoral mechanisms of BP control | - renin-angiotensin-aldostrone system
- vasopressin (ADH)
- epinephrine/norepinephrine
🗑
|
||||
| baroreceptors measure | - changes in heart rate
- rate of contraction
- vascular smooth muscle tone
🗑
|
||||
| the humoral mechanism that has a *major* role in BP control | renin-angiotensin-aldostrone system
🗑
|
||||
| process of the renin-angiotensin-aldostrone system | - renin released by kidneys
- renin converted to angiotension I in blood stream
- angiotension I converted to angiotension II in lungs
- angiotension II vasoconstricts and stimulates adrenal cortex
- adrenal cortex releases aldostrone
- Na+ retention
🗑
|
||||
| what is the trigger for renin release | - changes in extracellular fluid
- changes in sodium levels
- decrease in BP
- increase in sympathetic activity
🗑
|
||||
| what converts angiotension I to angiotesin II | angiotensin converting enzyme
🗑
|
||||
| target organ(s) of angiotension II | -smooth muscles of vessels
- adrenal cortex
🗑
|
||||
| function of aldostrone | increase salt and water retention by the kidneys (increasing BP as a secondary effect)
🗑
|
||||
| great long term regulation of BP | renin-angiotensin-aldostrone system
🗑
|
||||
| what is vasopressin | antidiuretic hormone
🗑
|
||||
| what is the trigger for ADH release | decrease in BP
🗑
|
||||
| what is ADH released from | posterior pituitary
🗑
|
||||
| what is the function of vasopressin | vasoconstriction
🗑
|
||||
| what is the target organ of vasopressin | - tubules of kidneys
- smooth muscle of arterioles
🗑
|
||||
| epinephrine an norepinephrine come from | the adrenal medulla (when stimulated by the sympathetic nervous system)
🗑
|
||||
| what is the function of the catecholamines | - vasoconstriction
- increase heart rate
- increase contractility
- increased BP is a secondary effect to the above functions
🗑
|
||||
| many blood pressure meds focus on what | increased sodium and water elimination by the kidneys
🗑
|
||||
| what is the etiology of hyperlipidemia | (multifactoral in nature)
bottom line: excess LDL and cholesterol levels in the blood
🗑
|
||||
| what is(are) the mechanisms of the hyperlipidemia | - excess lipids in blood
- genetic defects in apoprotiens
- low ldl receptor availability
- low hdl levels
🗑
|
||||
| why is excess lipids in blood stream (hyperlipidemia) a problem | it is a major contributor to atherosclerosis and risk factor for heart attack and stroke
🗑
|
||||
| what are some clinical manifestations of hyperlipidemia | - high ldl levels
- xanthomas
- appearance of atherosclerosis
🗑
|
||||
| what are xanthomas | cholesterol deposits (around tendons)
🗑
|
||||
| list the 5 types of lipoprotiens | - chylomicrons
- very-low-density lipoprotien (VLDL)
- intermediate-density lipoprotien (IDL)
- low-density lipoprotein (LDL)
- high-density lipoprotein (HDL)
🗑
|
||||
| which lipoprotein is good and which one is bad cholesterol | HDL is good, LDL is bad
🗑
|
||||
| what are the function of apoprotiens | play a role in mediating removal of lipids from blood stream
🗑
|
||||
| function of VLDL | carry triglycerides in blood stream
🗑
|
||||
| where are lipoproteins synthesized | small intestine and liver
🗑
|
||||
| what is the function of HDL | carries cholesterol away from peripheral tissue and back to the liver for excretion. this helps atherosclerosis and lowers risk
🗑
|
||||
| what is primary hyperlipidemia | - elevated cholesterol that develops independently of other health problems (ie skinny lifestyle blogger/influencer with 5 stents)
🗑
|
||||
| what is secondary hyperlipidemia | assosicated with other problems and behaviors (ie morbid obesity, decreased thyroid function)
🗑
|
||||
| familial hyperlipidemia | - autosomal dominant disorders
- deficiency/defective LDL receptors
🗑
|
||||
| heterozygous familial hyperlipidemia | LDL will be roughly 250-500 mg/dL
🗑
|
||||
| homozygous familial hyperlipidemia | LDL will be roughly 1000 mg/dL
🗑
|
||||
| what are three medication classes that can elevate lipids | - beta blockers
- estrogens
- protease inhibitors (HIV medication)
🗑
|
||||
| how is hyperlipidemia diagnosed | lipid panel labs
🗑
|
||||
| how is hyperlipidemia treated | - dietary and lifestyle changes (1st)
- pharmaceutical therapy (2nd)
🗑
|
||||
| list 4 risk factors for hyperlipidemia | - smoking
- HTN
- family history
- HDL < 40 mg/dL
🗑
|
||||
| list the 5 classes of hyperlipidemia drugs | - HMG CoA reductase inhibitors (statins)
- bile acid-binding resins
- cholesterol absorption inhibitor agents
- niacin
- fibrates
🗑
|
||||
| how do HMG CoA reductase inhibitors (statins) work to lower cholesterol | - reduce/block hepatic synthesis of cholesterol
🗑
|
||||
| how do bile acid-binding resins work to lower cholesterol | - bind and sequester cholesterol-containing bile acids
- usually used in adjunct to statin therapy
🗑
|
||||
| what drugs are part of the HMG CoA reductase inhibitors | all the statins
🗑
|
||||
| what drugs are in the class bile-acid-based resins | - cholestyramine
- colestipol (petal)
- colesevelam (welchol)
🗑
|
||||
| vitamin B3 | niacin (nicotinic acid)
🗑
|
||||
| how does niacin work to lower cholesterol | - block synthesis and release of VLDL by liver
🗑
|
||||
| what medications are part of the fibrate class | - fenofibrates
- gemfibrozil
🗑
|
||||
| what is the function of fenofibrates | lower VLDL
🗑
|
||||
| what is the etiology of atherosclerosis | - hardening of the arteries
- multifactoral causes
🗑
|
||||
| what is the mechanism of atherosclerosis | - fibrofatty lesions in lining of arteries (macrophages play a large role in this)
🗑
|
||||
| what are clinical manifestations of atherosclerosis | - usually many are not aware they have it until after a medical emergency presents itself
- is arterial stenosis
- production of ischemia
- sudden vessel obstruction (due to plaque hemorrhage or rupture)
(many others)
🗑
|
||||
| the most common arteries affected by atheroscerosis feed which organs | - brain
- heart
- kidneys
- legs
- small intestine
🗑
|
||||
| name at least 5 risk factors for atherosclerosis | - hyperlipidemia
- obesity
- smoking
- visceral fat
- DM I/II
- HTN
- increased age
- family history
- gender
- elevated CRP
- elevated serum lipoproteins
🗑
|
||||
| three lesion types of atherosclerosis | - fatty streak (mostly in children)
- fibrous atheromatous plaques
- complicated lesions
🗑
|
||||
| describe the fatty streaks | - thin, flat, yellow lines
- present in childhood
- asymptomatic
🗑
|
||||
| describe fibrous atheromatous plaques | the basic lesion of clinical atherosclerosis
--- increased size = increased occlusion
🗑
|
||||
| describe complicated lesions | - lesions that break open (hemorrhage, ulcer, or scar)
- thrombus formation (causes turbulence, occulsions, weakened arteries, and aneurysm developments)
🗑
|
||||
| Hypertension stage 1 definition | 130-139 OR 80-89
🗑
|
||||
| hypertension stage 2 definition | >= 140 OR >= 90
🗑
|
||||
| hypertensive urgency definition | >180 and or >120
🗑
|
||||
| hypertensive emergency definition | > 180 + organ damage and or >120 + organ damage
🗑
|
||||
| non-modifiable risk factors for HTN | -family history
- age related
- race
- some diseases (renal disease, renal artery stenosis, endocrine disorders (aldosteronism))
🗑
|
||||
| modifiable risk factors for HTN (name at least 5) | - high salt intake
- obesity
- excessive calorie intake
- alcohol abuse
- low potassium intake
- insulin resistance
- DMII
- hyperlipidemia
- Sleep apnea
- some drugs
🗑
|
||||
| tips for preventing HTN | - avoid processed foods
- drop 10 lb (if obesity is a factor)
- decrease alcohol abuse
- increase potassium (found in many fruits and veggies)
🗑
|
||||
| how potassium helps with HTN | - helps secrete sodium in kidneys
- suppresses the renin-angiotension- aldostrone system
🗑
|
||||
| prolonged HTN can lead to | - LVH
- nephrosclerosis (hypofunctions of glomerulous)
- worsened DMII neuropathy
- can also effect eyes, blood vessels, and kidneys and lead to target organ damage
🗑
|
||||
| how is htn diagnosed | - repeated BP measurements
- lab tests (to rule out possible primary causes)
🗑
|
||||
| how is HTN treated | - lifestyle changes (modifiable risk factors...1st)
- DASH diet (lost of fruits and veggies, whole grains, low dietary fats)
- weight loss
- increased physical activity
- medications
🗑
|
||||
| list the classes of HTN drugs | - diuretics
- ACE inhibitors
- ARBs
- calcium channel receptor blockers
🗑
|
||||
| what drugs are in the diuretics | thiazides
🗑
|
||||
| function of diuretics | - decreased CO, renal reabsorption of sodium (water follows sodium), peripheral vascular resistance
🗑
|
||||
| name the ACE inhibitors | the -prils (ramipril, lisinopril,
🗑
|
||||
| function of ACE inhibitors | prevent conversion of angiotensin I to angiotensin II
🗑
|
||||
| name the ARBs | the -sartans (losartan, valsartan, olmesartan)
🗑
|
||||
| function of the ARBs | prevent angiotensin II from binding to angiotension II receptors
🗑
|
||||
| function of the calcium channel receptor blockers | inhibit movement of calcium into the cardiac and vascular muscles
🗑
|
||||
| effects of the ACE inhibitors | - reduces vasoconstriction, aldosterone release, intrarenal blood flow, GFR
🗑
|
||||
| effects of ARBs | decreases peripheral resistance
🗑
|
||||
| effects of calcium channel receptor blockers | - decreased vasoconstriction, cardiac contractility, heart rate, cardiac output, venous return
🗑
|
||||
| what is the etiology of coronary artery disease | impaired cardiac blood flow
🗑
|
||||
| what are the mechanisms of coronary artery disease | - atherosclerosis
- myocardial ischemia
🗑
|
||||
| how is CAD diagnosed | - EKG changes
- stress testing
- cardiac cath
- angiography
- echo
- dopplers
- mri
- ct
🗑
|
||||
| risk factors for CAD | - smoking
- chronic htn
- diabetes
- obesity
- decreased physical activity
- increased LDL
- decreased HDL
🗑
|
||||
| main arteries of the heart | - left coronary artery (becomes the circumflex and left anterior descending)
- righte coronary arteries (posterior descending)
🗑
|
||||
| what are the determinants of myocardial oxygen demand (MVO) | - heart rate (mist important factor)
- left ventricular contractility
- systolic pressure/myocardial tension
🗑
|
||||
| what happens to cardiac oxygen demand with increase cardiac contractility | oxygen demand is increased
🗑
|
||||
| what does an EKG measure | - electrical potential of a cardiac cycle
🗑
|
||||
| what does a 12 lead EKG help diagnose | - conduction defects
- arrhythmias
- electrolyte imbalances
- drug effects
- genetic electrical or structural abnormalities
🗑
|
||||
| what is the function of stress testing | - determine how the heart functions under stress
🗑
|
||||
| what is the function of an echocardiogram | - structure and function of the heart
- mechanics of a heart beat
🗑
|
||||
| what is the function of a cardiac cath | an invasive procedure
🗑
|
||||
| name the two types of CAD | - acute coronary syndrome (ACS)
- chronic ischemic heart disease
🗑
|
||||
| this type of CAD covers a wide range of acute ischemic disease (from unstable angina to MI( | acute coronary syndrome (ACS)
🗑
|
||||
| what is chronic ischemic heart disease | - recurrent/transient episodes of myocardial ischemia and stable angina
🗑
|
||||
| what causes chronic ischemic heart disease | narrowing of coronary artery lumen through
- atherosclerosis
- vasospasms
🗑
|
||||
| types of atherosclerotic lesions | - fixed/stable plaque
- unstable/vulnerable plaque (high risk plaque)
🗑
|
||||
| what type of atherosclerotic lesion will produced stable angina | fixed/stable plaque
🗑
|
||||
| problems with unstable/vulnerable plaque | - can rupture
- can cause platelet adhesion
- thrombus formation
🗑
|
||||
| cardiac function is determined by | how the supply (oxygenated blood) meets the demand (myocardial demand for Oxygen)
🗑
|
||||
| what is stable angina | - chest pain/tightness/discomfort and or shortness of breath with exertion and relieves with rest or nitro
🗑
|
||||
| what does stable angina mean | > 70% stenosis of a coronary artery
🗑
|
||||
| what is unstable angina | chest pain/tightness/discomfort without exertion and does NOT relieve with nitro or rest
🗑
|
||||
| what does unstable angina mean | total occlusion of at least one coronary artery
🗑
|
||||
| layman's term for myocardial infarction | heart attack
🗑
|
||||
| (physiologically) what is a myocardial infarction | portion of myocardial death
🗑
|
||||
| clinical manifestations of acute MI | - unstable angina (sometimes present in jaw, left arm, or neck)
- dyspnea
- nausea/vomiting
- sweating
- EKG changes
- elevated troponin
- elevated creatine kinase MB (CKMB)
- other visible signs of distress
🗑
|
||||
| in an MI situation, what is the goal of a medical provider | reprofuse the myocardium
🗑
|
||||
| the goal for medical personnel is to reprofuse the myocardium after an MI, how is this accomplished | - thrombolytic drugs
- surgical procedures
- other treatments
🗑
|
||||
| thrombolytic drugs used for MI | -streptokinase
- tissue plasminogen activator (tPA)
🗑
|
||||
| some invasive procedures to treat an MI | - Cardiac stenting
- angioplasty
- CABG
🗑
|
||||
| list some treatments used to help treat an MI | - Oxygen
- ASA
- nitrates
- pain meds
- antiplatelet therapy
- anticoagulant therapy
- betablockers
🗑
|
||||
| death after an MI | - within 1 hour after 1st symptom
- caused by fatal arrhythmias
🗑
|
||||
| treatment approaches for CAD | - decrease heart demand for oxygen
- increase vasodilation of coronary vessels
🗑
|
||||
| function of beta blockers with CAD | decreased heart demands for Oxygen
🗑
|
||||
| function of calcium channel blockers with CAD | - mostly decrease heart demand for Oxygen
- also helps with decreasing vasospasms
🗑
|
||||
| function of nitrates with CAD | - vasodilate coronary arteries
- decreases both preload and afterload
🗑
|
||||
| describe hypertrophic cardiomyopathies | _ LVH with disproportionate thickening of interventricular septum
- most common cause of death of young athletes
🗑
|
||||
| describe dilated cardiomyopathies (DCM) | - common cause of heart failure
- leading indication for heart transplant
- dilation of ALL chambers
- decreased wall thickness
- decreased systolic function
🗑
|
||||
| describe restrictive cardiomyopathy | - infiltrative processes within myocardium
- caused by
----- amyloidosis
----- sarcoidosis
- can be right or left
🗑
|
||||
| describe myocarditis (inflammatory cardiomyopathy) | - viral causes (coxsackie B virus)
🗑
|
||||
| signs and symptoms of | - fever
- myalgias
- dyspnea on exertion
- hemodynamic collapse
- sudden death
🗑
|
||||
| what are arrhythmias | - abnormal heart rhythms
- uncoordinated electrical conduction = uncontrolled contraction
🗑
|
||||
| normal sinus rhythm | 60-100 bpm
🗑
|
||||
| bradycardia | < 60 bpm
🗑
|
||||
| tachycardia | > 100 bpm
🗑
|
||||
| list some atrial arrhythmias | - PAC's
- multifocal and focal atrial tachycardia
- a flutter
- a fib
🗑
|
||||
| list some ventrical arrhythmias | - PVC
- V. Tach
- V. fib
🗑
|
||||
| what is multifocal atrial tachycardia | - irregular p wave intervals
- seen in pulmonary disease
🗑
|
||||
| describe paroxysmal atrial tachycardia | - focal atrial tachycardia
- starts and ends suddenly
🗑
|
||||
| describe a flutter | - reentrant circuit that is on a loop
- atrial rate 200-400 bpm
🗑
|
||||
| describe a fib | - reentrant circuits spinning around
- no discernible P waves
- most common chronic arrhythmia
🗑
|
||||
| describe pvc | - ectopic ventricular pacemaker
- compensatory pause
----- after pvc and prior to the normal sinus rhythm
🗑
|
||||
| describe vtach | - reentrant circuit
- seen with
----- MI
- rate 70-250 bpm
- dangerous rhythms
🗑
|
||||
| describe v fib | - multiple reentrant circuit
- more uncoordinated than Vtach
- (without intervention) results in sudden death
🗑
|
||||
| etiology of heart failure | - functional/structural impairment of ventricular filling/ejection
- low cardiac input/output
🗑
|
||||
| diseases that can cause heart failure | - CAD
- HTN
- Dilated cardiomyopathy
- valvular diseases
🗑
|
||||
| mechanisms of systolic heart failure | - impaired ejection during systole
- inability to contract efficiently
- produce volume overload
🗑
|
||||
| mechanism of diastolic heart failure | - impaired filling capacity during diastole
- impeded expansion of ventricle
-
🗑
|
||||
| mechanism of right sided heart failure | - decreased ability of right ventricle
- peripheral edema
- measured through daily weight checks
- most commonly caused by left ventricular failure
🗑
|
||||
| mechanism of left sided heart failure | - decreased ability for blood to be ejected from left ventricle
- decreased cardiac output
- blood accumulates in heart and lungs
🗑
|
||||
| what are the most common causes for left sided heart failure | -MI
- HTN
- valve stenosis or regurgitation
------ aortic valve
------ mitral valve
🗑
|
||||
| what are the clinical manifestations of right sided heart failure | - peripheral edema
- hepatomegaly
- ascites
- enlarged spleen
🗑
|
||||
| what are the clinical manifestations of left sided heart failure | - blood accumulation in the heart
- blood accumulation in the lungs
🗑
|
||||
| what are some clinical manifestations of heart failure (in general) | - SOB
- fatigue
- weakness
- orthopnea (SOB while lying flat)
- paroxysmal nocturnal dyspnea (SOB/cough at night)
- limited activity tolerance
- fluid retention
- increased jugular venous pressure
- ascites
- cyanosis
🗑
|
||||
| list some mechanisms for heart preservation during heart failure | - Frank-starling mechanism
- activation of the SNS
- renin-angiotensin-aldosterone mechanism (vasoconstriction)
- natriuretic peptides
- endothelins
- myocardial hypertrophy + remodeling
🗑
|
||||
| how does the frank-starling mechanism help preserve the heart | - increases muscle stretch (intropy)
🗑
|
||||
| how does activation of the SNS help preserve the heart | - more immediate
- increases heart rate
- increases cardiac output
🗑
|
||||
| how doe the renin-angiotensin-aldosterone mechanism help preserve the heart | - decreases cardiac output
- decreases renal blood flow
- increases sodium and water retention
🗑
|
||||
| name the two natriuretic peptides | - atrial natriuretic peptide (ANP)
- brain natriuretic peptide (BNP)
🗑
|
||||
| how do the natriuretic peptides preserve the heart | - both are diuretics (release sodium)
- both (ANP and BNP) are elevated in heart failure patients
🗑
|
||||
| how do endothelins help preserve the heart | - vasoconstrictor peptides
- from the endothelial cells
🗑
|
||||
| how is heart failure diagnosed | - H+ P
- lab studies
- ekg studies
- CXR studies (shows enlarged heart)
- echo studies
🗑
|
||||
| how do lab tests show heart failure | they can show
- anemia
- electrolyte imbalances
- chronic liver congestion
🗑
|
||||
| how doe echos diagnose heart failure | - assess left ventricle wall
------ motion
------ thickness
------ chamber size
- valve function
- heart defects
- ejection fraction
- pericardial disease
🗑
|
||||
| how does a physical help diagnose heart failure | - heart sounds
- bp level
- jugular vein congestion
- lung congestion
- BLE edema
🗑
|
||||
| how does a CXR help diagnose heart failure | - measures heart size
- measures heart shape
- pulmonary vasculature
🗑
|
||||
| what are the goals of heart failure treatment | - relieve symptoms
- improve quality of life
- reduce/eliminate risk factors
🗑
|
||||
| how is heart failure treated | - exercise training
- sodium and fluid restriction
- weight management
- pharmacological assistance
🗑
|
||||
| list the pharmacological classes used to help treat heart failure | - diuretics
- ACE inhibitors
- angiotensin II receptor blockers
- beta blockers
- digoxin
- vasodilators
🗑
|
||||
| function of diuretics with heart failure treatment | - fluid excretion
- decreased preload
🗑
|
||||
| the function of both ACE inhibitors and angiotensin II receptor blockers in heart failure treatment | - prevent angiotensin from being converted to angiotensin II
- decrease vasoconstriction
- decrease aldosterone production
- Na and water retention in kidneys
- dilates arteries
- decreases afterload
🗑
|
||||
| the function of beta blockers in treating heart failure | - decrease left ventricular dysfunction
- prevents actuation of SNS
- decrease ventricular rate
🗑
|
||||
| the function of digoxin in treating heart failure | - increase force and strength of ventricular contraction
- decreased heart rate
- increased diastolic filling time
🗑
|
||||
| etiology of cardiogenic shock | - the heart fails to pump properly
- most common cause is an MI
🗑
|
||||
| what are the mechanisms of cardiogenic shock | - decreased CO
- hypotension
- hypoperfusion (low oxygen perfusion)
- tissue hypoxia
- decreased SV
- increased vascular resistance
- increased fluid retention (renin-angiotensin-aldosterone sys)
🗑
|
||||
| clinical presentations of cardiogenic shock | - hypoperfusion (decreased O2 levels)
- hypotension
- cyanosis
- decreased urine output
- neurological changes (poor cerebral perfusion)
🗑
|
||||
| treatment of cardiogenic shock | - improve CO
- decrease workload of myocardium
- increased coronary perfusion
- maintain fluid load
- correct/prevent arrhythmias and pulmonary edemas
- increase vasodilation
- increase BP
- decrease ventricular wall tension
🗑
|
||||
| medication used for cardiogenic shock | - vasodilators
----- nitroprusside
----- nitroglycerin
🗑
|
||||
| function of vasodilator medications in cardiogenic shock patients | - increased O2 delivery to myocardium
- decreased venous return
🗑
|
Review the information in the table. When you are ready to quiz yourself you can hide individual columns or the entire table. Then you can click on the empty cells to reveal the answer. Try to recall what will be displayed before clicking the empty cell.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Created by:
kandriot
Popular Pathology sets