Exam 1 Edema, Electrolytes, A/B, Cardiac Flashcards
(384 cards)
1
Q
What barorecptors monitor BP?
A
Carotid sinus and aortic arch
2
Q
What apparatus monitors pressure changes?
A
Juxtaglomerular
3
Q
The baroreceptors of heart activate what mechanisms?
A
Neural, RAAS, ANP, ADH
4
Q
How does the body regulate fluid volume and composition both intracelluarly and extracellularly?
A
By regulating volume and composition of blood
5
Q
What is the dominant ECF cation?
A
Na+
6
Q
What is responsible for 90-95% of osmotic pressure in ECF?
A
Na+
7
Q
What does osmolality measure?
A
Concentration
8
Q
What does osmolality regulation depend on?
A
How much water is present
9
Q
What is the primary hormonal control of osmolality?
A
ADH
10
Q
What forces favor filatration?
A
Capillary hydrostatic pressure (blood pressure)
Interstitial oncotic pressure (water-pulling)
11
Q
What forces favor reabsorption?
A
Plasma oncotic pressure (water-pulling)
Interstitial hydrostatic pressure
12
Q
ECF volume may vary even if osmolality of ECF is maintained? T or F
A
True
13
Q
What is accumulation of fluid within the interstitial spaces?
A
Edema
14
Q
What are causes of edema?
A
Increase in hydrostatic pressure
Losses or dim production of plasma albumin
Increases in capillary permeability
Lymph obstruction
15
Q
What are the local clinical manifestations of edema?
A
Limited to site of trauma
Includes cerebral, pulmonary, pleural effusion, pericardial effusion, ascites
16
Q
What are the generalized clinical manifestations of edema?
A
More systemic
Dependent edema accumulates in a gravity dependent manner
17
Q
Other clinical manifestations of edema
A
Increased distance for diffusion of O2 so less gets to cells
Decreased blood flow leads to poor wound healing
Dehydration due to fluid not available for metabolis or perfusion
18
Q
What is an example of edema?
A
Fluid sequestration following severe burns leads to shock
19
Q
What is tightly regulated ECF due to influences on volume?
A
Na+
20
Q
Small quantities of Na+ are lost in what?
A
Sweat= water, Na+, urea, Cl-, K+, NH3
21
Q
What happens when Na+ is low and H2O moves into cells?
A
Hypotonic- cell swell
22
Q
What happens when Na+ is too high and water moves out of cell?
A
Hypertonic solution- cell shrink
23
Q
What happens with Na+ and water are stable in the cells?
A
Isotonic solution-no change
24
Q
What are the 3 fluid compartments in the brain?
A
Blood
ECF and ICF
CSF
25
Is there a fixed volume in the cranium?
Yes
26
If you increase the fluid in one compartment in brain then what must happen to other two compartments?
Must decrease
27
Hyponatremia alters what function?
Neurlogic
28
Rapid shrinking can do what to the brain?
Tear vessels and cause hemorrhage
29
Rapid swelling can do what to the brain?
Herniation
30
What factors regulate Na+ retention?
Estrogens
Glucocorticoids
Osmotic diuretics
Poorly reabsorbed anions
Diuretic drugs
Dopamine
31
How does glucocorticoids regatulate Na+ retention?
Increase Na+ retention
32
How do osmotic diuretics regulate Na+ retention?
Decrease Na+ retention
33
How does poorly reabsorbed anions regulate Na+ retention?
Decrease Na+ retention
34
How does dopamine regulate Na+ retention?
Increases Na+ retention
35
Where is 98% of our total body K+ found?
Intracellular
36
What is circumferential range of K+?
0.3 range of 4.2 (3.9-4.5)
37
What is the major determinant of intracellular volume?
K+
38
What can serve as a outflow site for excess extracelluar fluid during hyperkalemia or hypokalemia?
Cells
39
What is 1st line of defense against changes in K+?
Redistribution
40
What does K+ establish with the heart?
Resting membrane potential
41
Low K+ will do what to the RMP?
Increase RMP (make it more negative)
Decrease excitability
42
High K+ will do what to the RMP?
Decrease RMP (makes it more pos)
Increase excitability
43
Acidosis will do what to the K+?
Increase it (hyperkalemia)
44
Alkalosis does what to the K+?
Lower K+ (hypokalemia)
45
K+ effects what ezymes?
Ones involved in carb metabolism and electron transport
46
How does increased aldosterone effect K+?
Causes K+ excretion
Increase permeability of luminal membrane permeability to K+
47
What disorders of aldosterone synthesis affect K+ regulation?
Addison’s Dx
Cohn’s Syndrome
48
How does K+ regulation effect tubular flow rate?
Increased tubular flow rate
49
The higher the concentration gradient then the more or less K+ is lost?
More
50
Hyperkalemia results from what?
Increased intake
Renal failure
Crushing injuries
Acidosis
51
What are symptoms of hyperkalemia?
muscular weakness
Irritability
Vent fib.
EKG changes
52
Hypolakemia results from what?
Excessive loss (diarrhea) or decreased intake
Kidney dx
Certain diuretics-lasix
53
Hypokalemia causes what symptoms?
Muscle fatigue
flaccid paralysis
mental confusion
Increased urine output
EKG changes
54
What is 99% of Ca+ found?
Bone
55
What stimulates osteocytes to deposit Ca+ within bone?
Calcitonin (CT)
56
What does Parathyroid hormone cause?
Bone resorption (osteoclasts)
Increase rental tubular reabsorption
Stimulates Vit D which increases intestinal absorption of Ca+
57
Acidosis frees Ca+ from what?
Proteins
58
Alkalosis will increase or decrease the percent of Ca+ bound to proteins?
Increase
59
How is most Ca+ excreted from body?
Feces (900-1000 mg/day)
60
Metabolic acidosis increases or decreases in Ca+ reabsorption?
Increases
61
Metabolic alkalosis increases or decreases Ca+ reabsorption?
Decreases
62
How does hypercalcemia affect the neuromuscular excitability and heart?
Causes neuromuscular excitability depression
Cardiac arrhythmias
63
Hypocalcemia has what affect on neuromuscular and heart?
Increase nerve and muscle excitability
Tetany
64
What changes the RMP?
K+
65
How does low K+ affect heart?
Decrease excitability
RMP more neg
Harder to get AP
66
How does high K+ affect RMP?
Increase excitability
Makes RMP more pos
Easily to excite and get AP
67
What does Ca+ effect in heart?
Threshold
By affecting Na+ entry into cells
68
How does high Ca+ affect threshold?
Increase threshold
Make cells less excitable
Harder to get AP
69
What are 3 ways the body regulates pH?
Chemical buffers (bicarbonate, proteins, phosphate)
Lungs
Kidneys
70
What is the main buffer in the ECF?
Bicarbonate
71
What is respiratory acidosis?
Low pH
High CO2
72
What is respiratory alkalosis?
High pH
Low CO2
73
What is metabolic acidosis?
Low pH
Low HCO3
74
What is metabolic alkalosis?
High pH
High HCO3
75
Normal anion gap?
8-16
76
What is normal anion gap?
Increased Cl-
Sum of Cl- and HCO3 normal
AKA hyperchloremic acidosis
77
Causes of normal anion gap ?
Diarrhea (most common)
Renal tubular dysfunction
Ammonia chorlide ingestion
Carbonic anhydrase inhibitors
78
What is increased anion gap?
Normal Cl-
Increased levels of unmeasured anions
79
What are examples of increased anion gap?
MUD PILERS
Methanol poisoning
Uremia (renal failure)
DKA (ketoacidiosis, starvation)
Pa-P-Aldehyde intoxication
Isoniazid
Lactic acidosis
Ethylene glycol poisoning (antifreeze)
Renal failure
Salicylate poisoning
80
Where is two thirds of the body’s water?
Intracellular fluid (ICF)
81
Where is one third of the body’s water?
Extracelluar fluid (ECF)
82
What are the two main components of the ECF?
Interstitial fluid and intravascular fluid (plasma/blood)
83
What is the standard value for total body water (TBW)?
60% of weight of 70 kg adult male
84
Hormonal regulation of Na+ balance is mediated by what?
Aldosterone
85
What happens in the kidneys when the blood pressure or blood volume is low?
Renin is released to convert AGI to AGII
86
What are the two main functions of AGII?
Vasoconstriction (increases BP)
Simulates secretion of aldosterone (promote Na+ and H20 reabsorption)
87
What is a major factor in regulating potassium?
Aldosterone
88
How does insulin affect K+?
Moves K+ into cells to lower K+ in blood by stimulating NaK pump
89
What provides the most efficient regulation of K+ balance over time?
Kidneys
90
What do principal cells in collecting duct do?
Secrete K+
91
What do intercalated cells in collecting duct do?
Reabsorbed K+
92
What hormone gets secreted due to low levels of Ca+?
Parathyroid hormone
93
What is anemia?
Decrease in # of circulating RBCs or decrease in quality or quantity of HGB
94
What is anemia a sign of?
Another underlying problem
It is not the primary issue
95
What are the causes of anemia?
Altered RBC production
Blood loss
Increased RBC destruction
Combination of all three
96
What is anemia classification based on?
Morphology
97
What is the size of RBC identified by?
Terms that end in “-cytic”
Macrocytic, Microcytic, normocytic
98
What is the hemoglobin content identified by?
Terms that end in “-chromic”
Normonchromic and hypochromic
99
What type of anemia is B12 or folate deficiency?
Macrocytic-Normochromic
100
What type of anemia is iron deficiency or thalassemia?
Microcytic-Hypochromic
Hgb don’t form properly
101
What type of anemia is hemorrhage, hemolytic, aplastic?
Normocytic-Normchromic
102
What is the genetic dx with low O2 and hgb forms irregular shape which clogs capillaries?
Sickle cell dx
103
What are the manifestations of anemia?
Hypoxia- fatigue, weakness, dyspnea, angina
104
How does the body compensation for anemia?
Attempts to increase cardiac output by increasing rate and strength of contraction
105
What is polycytemia?
Increase RBC production
106
What is difference between relative and absolute polycythemia?
Relative- blood thicker due to dehydration for example
Absolute- issue with erythropoietin so increases it
107
What is the issue with anemia in cardiac dx patients?
Increase HR to compensation can be bad for these pts
108
What is most compensation of anemia related to?
Cardiac
109
What happens in anemia?
Decrease O2 carrying capacity (hypoxemia)
Leads to tissue hypoxia
110
What is anemia of chronic dx?
Mild to moderate anemia from decreased erythropoiesis
111
What are some pathological mechanisms of anemia of chronic dx?
Decreased erythrocyte life span
Suppressed production of erythropoietin
Ineffective bone marrow response to erythropoietin
Altered iron metabolism
112
What is aplastic anemia?
Pancytopenia (reduction or absence of all 3 types of blood cells)
RBC, WBC, PLT
113
What type of disorders are most aplastic anemia?
Autoimmune disorders
Some are due to chemicals, drugs, physical agents
114
What is pathophysiology of aplastic anemia?
Hypocelluar bone marrow that has been replaced with fat
115
What are the signs of aplastic anemia?
Hypoexemia
Pallor (brownish pigment of skin)
Weakness
Fever
Dyspnea
Rapidly developing signs of hemorrhaging if plts affected
116
What is aplastic anemia a failure or suppression of?
Failure or suppression of bone marrow to produce adequate amounts of blood cells
117
What anemia is common due to drug effects?
Aplastic anemia
118
What drugs are known to cause aplastic anemia?
ABX (Chloramphenicol)
Anticonvulsants (Phenytoin, Mephenytoin)
Anti-inflammatories (ibuprofen)
Benzene
119
What is hemolytic anemia? What are 2 types?
Accelerated destruction of RBCs
Can be congenital (newborn) vs acquired (drug induced)
120
What is autoimmune hemolytic anemia?
Autoantibodies against antigens normally on surface of erythrocytes
121
What is a form of immune hemolytic anemia that is the result of allergic reaction to foreign antigens?
Drug induced hemolytic anemia
Called hapten model
122
What drugs can cause drug induced hemolytic anemia?
ABX
Penicillin
Cephalosporins (more than 90%)
Hydrocortisone
123
What is the drug induced hemolytic anemia called?
Hapten model
124
What is the hapten model with drug induced hemolytic anemia?
IgG antibody against drug or against unique antigen formed by interface of drug and erythrocyte protein is formed and binds to erythrocyte at normal body temperature
125
Where does hemolysis occur with drug induced hemolytic anemia?
Extravascular
126
What can rapidly resolve drug induced hemolytic anemia?
Cessation of drug administration
127
What are signs of drug induced hemolytic anemia?
Asymptomatic
Jaundice (icterus)
Aplastic crisis
Splenomegaly
128
What type of anemia is commonly noted in presence of CHF?
Anemia of chronic dx
129
How is hemolytic anemia divided into categories?
Congenital or acquired
Acquired is drug induced form
130
How does hemolytic anemia occur?
Occurs in blood vessls (intravascular) or lymphoid tissues (extravascular) that filter blood
Spleen or liver
131
What is intravascular hemolysis?
Least common
Caused by physical destruction of RBCs in circulation
132
What is extravascluar hemolysis?
Results from removal of damaged or opsonized RBCs by cells of mononuclear phagocyte system (MPS)
133
What is the most common type of megaloblastic anemia caused by vitamin B12 deficiency?
Pernicious anemia
134
What is folate deficiency anemia?
Impaired DNA synthesis secondary to folate deficiency cause megaloblastic cells with clumped nuclear chromatin
Folic acid is essential for RNA and DNA synthesis
135
What type of anemia is iron (fe) deficiency anemia?
Microcytic-Hypochromic anemia
136
What is the most common type of anemia worldwide?
Iron deficiency anemia
137
Who has higher risk for iron deficiency anemia? Males or females
Females
138
What are the 2 main causes of iron deficieny anemia?
Inadequate dietary intake
Excessive blood loss
(There is not intrinsic dysfunction of iron metabolism)
Both deplete iron stores & reduce iron metabolism
139
What is another cause of iron deficiency anemia?
Due to metabolic or function iron deficiency in which various metabolic disorders lead to either insufficient iron delivery to bone marrow or impaired iron use within marrow
140
What is the common cause of iron deficiency anemia in developed countries?
Pregnancy and chronic blood loss
141
Iron in the form on hgb is in constant demand by the body? T or F
True
142
How does blood loss affect iron?
Disrupts balance by creating need for iron which depletes iron stores more rapidly to replace iron lost from bleeding
143
How is iron deficiency related to supply and demand?
Occurs when demand for iron exceeds the supply of iron
Develops more slowly through 3 overlapping stages
144
What are the stages of iron deficiency anemia?
Stage 1: body’s iron stores are depleted (hgb content normal)
Stage 2: iron transport to bone marrow decreases
Stage 3: small hgb deficient cells enter circulation to replace normal age RBCs that are removed from circulation (s/sx occur)
145
What are signs of iron deficiency anemia?
Pallor skin and eyes
Brittle nails with spoon shape
Glossitis (tongue bald appearance with loss of papillae)
146
What converts fibrinogen to fibrin?
Thrombin
147
Where do we see most deficiency in clotting cascade?
Near the end of clotting cascade
Rarely see in beginning with TF
148
What is Vit C deficiency?
Lack of stable collagen
149
What patients have Vit C deficiency?
elderly
Alcoholics
150
What does hepatic failure cause?
Depletion of clotting factors
151
Where are almost all clotting factors made?
Liver
152
What is Vit K deficiency?
Depletion of factors 2 (prothrombin), 7, 9, 10, and protein C & S
II, VII, IX, X
153
What is Vit K deficiency due to?
Fat malabsorption due to lack of bile secretion
154
What is hemophilia A?
Deficiency of factor VIII (8)
155
What is hemophilia B?
Deficiency of factor IX (9)
156
What hemophilia is more common? A or B
A
157
What is thrombocytopenia?
Low number of plts
Bleeding in small capillaries and blood vessels
Usually autoimmune disorder
158
What is factor V Leiden mutation?
Mutation (R506Q) in heavy chain of factor V
Resistant to cleavage by activated protein C
159
What does Factro V Leiden mutation result in?
Hypercoagulable state
Most common genetic risk factor for thrombosis in caucasians
160
What are causes of thrombocytopenia? (Low plts)
Hypersplenism
Autoimmune dx
Hypothermia
Viral or bacterial infections that can cause DIC or HIT
161
What are the two types of thrombocytopenia?
ITP (immune thrombocytopenia purpura)
TTP (thrombotic thrombocytopenia purpura)
162
What is IgG antibody that targets platelets glycopteins and signs ?
immune thrombocytopenia purpura (ITP)
Petechia, purpura, progressing to major hemorrhage
163
What is a thrombotic microangiopathy due to dysfunction of metalloproteinase ADAMTS13 enzyme?
Thrombotic thrombocytopenia purpura (TTP)
164
What is essential (primary) thrombocythemia?
Too many plts
>600,000 plts
Myeloproliferative disorder of plt precursory cells
Megakaryocytes in bone marrow are produced in excess of
165
What does platelet disorders result from?
Platelet membrane glycoprotein and von Willebrand factor deficiencies
Congenital or acquired
166
What is Virchow’s Triad that contribute to thrombosis?
-Endothelia injury (causes HTN)
-Alterations/stasis in normal blood flow (causes atherosclerosis, valvular disorders, stasis)
-Hypercoagulability (increase plt function or increase clotting)
167
What issues are associated with thrombosis?
Embolism
Infarction
DIC
168
What is a complex acquired disorder in which clotting and hemorrhage occur simultaneously?
DIC (Disseminated Intravascular Coagulation)
169
What happens with DIC?
Sudden onset of widespread thrombi in microcirculation with rapid consumption of plts and coagulation factors
Fibrinolysis is activated
170
What is DIC unable to control?
Unable to control thrombi
171
What is the primary initiator of DIC?
Endothelial damage
172
What is the result of DIC with increase protease activity?
Result of increase protease activity in blood caused by unregulated generation of thrombin with subsequent fibrin formation and either accelerated or diminished fibrinolysis
173
What does DIC result in?
Ischemia and hypoperfusion
Clot a lot then bleed a lot
174
What increases in DIC?
Fibrin degradation product (FDP) and D-dimer levels which downregluates clotting
But causes bleeding
175
What is mortality rate and treatment of DIC?
High mortality rate
TXT: try to remove stimulus
176
What are signs of DIC?
Bleeding from venipuncture sites, arterial lines
Purpura, petechia, hematomas
Symmetric cyanosis of fingers and toes
177
What are conditions associated with DIC?
Metastatic cancer
Acute bacterial and viral infections
Certain parasitic dx (malaria)
Sepsis/septic shock
Massive trauma
Burns
Products of conception
178
How do the conditions associated with DIC begin it?
Damage to endothelium
179
How does a patient get DIC?
-Due to initial endothelium damage leading to inflammatory cascade and massive activation of clotting cascade
-Widespread microvascular thrombisis which depletes factors
-Followed by bleeding due to depletion of factors and fibrinolysis
180
How does patient transition from clotting to bleeding with DIC?
Stage 1: overactive clotting due to endothelium damage activating clotting cascade
Stage 2: run out of clotting factors and plts which leads to massive bleeding
181
What determines the clinical course of DIC?
Intensity of stimulus, host response, comorbidities
182
What is laboratory evidence of DIC?
1. Clotting activation
2. Fibrinolytic activation
3. Coagulation inhibition consumption
4. End organ damage/failure
183
What is the most common condition associated with DIC?
Sepsis
184
How does sepsis cause DIC?
Gram neg, gram pos organisms, or fungi damage vascular endothelium
Gram neg are primary cause of damage
185
Does DIC cause local or widespread activation of coagulation cascade?
Widespread leading to clotting everywhere
186
What is the common pathway for DIC?
Excessive and widespread exposure to TF (tissue factor)
187
What are cause release of TF with DIC?
Cytokines
188
How does bleeding locations occur with DIC?
Bleeding at 3 or more unrelated sites
189
Which is more evident in DIC? Thrombosis or hemorrhage
Hemorrhage because it is more extensive and first observation
Sign of thrombosis are not always evident
190
What is hemolytic dx of the newborn due to?
Occurs if antigens on fetal RBCs differ from antigens on mom RBCs
191
What is patho of hemolytic dx of newborn?
Mom and fetus blood type different
Mom’s blood forms antibodies to fetal RBCs
Not problem with first pregnancy
Problem is with subsequent pregnancies
192
What is the patho of sickle cell dx?
Deoxygenation of RBCs causing them to assume abnormal shape due to Hb S in cells
193
What is chartacterized by intimal lesions called atheromas or fibrofatty plaques which protrude into and obstruct vascular lumens weakening underlying tunica media?
Atherosclerosis
194
What contributes to more mortality (50%) in western world than any other disorder?
Atherosclerosis
195
Who ends up with some plaque development?
Everyone
196
What are the 3 principle components of plaque?
Cells
ECM
Lipid
197
What are the cells of plaque made up of?
Macrophages
Smooth muscle
Lymphocytes
198
What is the primary cell in plaque?
Macrophages aka foam cells
199
What is the ECM (extracellular matrix) of plaque made of?
Collagen
200
What indicates the stability of plaque?
Collagen
More stable then the more collagen
201
What does the lipid component of plaque contain?
LDL
Oxidized LDL
202
What is worst: LDL or oxidized LDL?
Oxidized LDL
203
What happens with oxidized LDL?
Becomes free radical meaning extra e- present
Steals e- from others cells making them unstable
204
Is a stable plaque good or bad?
Good
No acute events will occur
205
What happens when stable plaque is disrupted?
Form blood clot acutely
206
What is the layers of plaque?
Fibrous cap on top (lesions develop and cells die underneath)
Necrotic center underneath
207
What are factors that induce or promote atherogenesis?
-Endothelial injury that alters normal homeostasis of endothelium
-Continuing inflammatory response
-Cyclic accumulation of cells and lipids
208
What are possible causes of endothelial injury that include common risk factors for atherosclerosis?
Smoking
HTN
DM
Increased LDL (hyperlipidiemia)
Decreased HDL
Autoimmunity
Obesity
209
What is the progression of atherosclerosis?
1. Damaged endothelium
2. Fatty streak
3. Fibrous plaque
4. Lesion
210
What does damaged endothelium occur in atherosclerosis?
Injured endothelial cells become inflamed and cannot make normal amts of antithrombotic and vasodilating cytokines
211
How does DM, smoking, and HTN cause atherosclerosis?
Contribute to increased LDL oxidation which causes toxic and cause smooth muscle proliferation
212
What do macrophages do?
Engulf the LDL
213
What happens when the foamy macrophages filled with LDL accumulate in significant amounts?
Fatty streak develops
214
What happens when fatty streaks produce more oxygen radicals and cause damage to vessel wall?
Smooth muscle cells proliferate, produce collagen cap, and form fibrous plaque over fatty streak
215
What are fibroblasts?
Cells that make collagen
216
What happens with fibrous cap thins?
-Plaque/cap will rupture which initiates clotting cascade and forms a thrombus
-Thrombus may occlude vessel leading to ischemia and infarction
217
What are the potential consequences of atheroclerosis?
-Narrow vessel leads to ischemia (Long term)
-Plaque hemorrhage or rupture caused by vessel obstruction (Acute)
-Thombosis lead to embolism (Acute)
-Aneurysmal dilation due to weak vessel wall
218
How does atherosclerosis progress?
In a variety of ways
219
What is the leading coronary artery & cerebrovascular dx?
Atherosclerosis
220
What is atherosclerosis from?
Elevated plasma cholesterol/LDL levels
221
What is the progression of plaque in atherosclerosis?
Lesions progress from endothelial injury to fatty streak to fibrotic plaque to complication lesion
222
What is the main cause of atherosclerosis plaque devleopment?
Endothelial cell injury
Imbalance btw proinflammatory and anti-inflammatory mediators
223
What is definition of HTN?
BP > 140/90
224
What is primary HTN?
HTN is issue with no other underlying conditions
Complicated interaction btw genetics and environment
225
What is the pathogenesis of HTN?
Increase CO
Increase peripheral resistance; increases afterload
Kidneys, RAAS, SNS all play a role
226
What are consequences of HTN?
Vessel injury
Prolonged vasoconstriction
Target organ dx
227
What is Liddle syndrome?
Genetic condition that leads to extreme HTN before puberty and into 20s
Defect in epithelial NA+ channel so not responsive to aldosterone
228
What does HTN result from?
Na+ retention and elevated BP
229
What does sustained HTN lead to?
Vascular remodeling (hylaine sclerosis and atherosclerosis)
230
What does vascular remodeling lead to?
Retinal changes
Renal dx
Cardiac dx (CAD, CHF)
Neurological dx (stroke, dementia)
231
What is SNS stimulation in HTN caused by?
Physiologic stress
232
What is the role of the SNS in leading to HTN?
Causes:
increase HR and peripheral resistance
Increase insulin resistance (endothelial dysfunction)
Vascular remodeling (narrow vessels)
Procoagulant effects
233
What factors lead to increased Na+ retention? (Decreased renal salt excretion so shift in pressure natriuresis relationship)
Genetics
Increase SNS
Increase RAAS
Endothelial dysfunction
Dysfunction of natriuretic hormones
Obesity
Renal glomerular and tubular inflammation
Insulin resistance
Increase Na intake
Decreased deitary K+, Mag, Ca+
234
What is the pressure-natriuresis (PN) relationship and how is it shifted in HTN?
PN is abnormal because Na+ excretion is the same as in normotensive despite increased BP
235
What hormones dysfunction with HTN?
Natriuretic hormones (ANP, BNP, CNP) which are unable to induce diuresis
Cause increase in vascular tone and shift PN relationship
236
What happens when there is inadequate natriuretic function?
Serum levels of natriuretic peptides increase which are linked to increased risk for vent hypertrophy, atherosclerosis, HF
237
What does salt retention lead to?
Salt retention leads to water retention and increases blood volume which causes increases in blood pressure
238
How does obesity play a role in developing HTN?
Causes change in adipokines (leptin and adiponectin) and is associated with increased activity of SNS and RAAS
239
What are the manifestations of HTN?
Atherosclerosis and LV hypertrophy
240
What is LV hypertrophy a risk factor for?
Ischemic heart dx
Arrhythmias
CHF
Death
241
What is one of the main long term consequence of HTN?
Ventricular remodeling
242
What is ventricular remodeling and ultimately result in?
Involved both SNS and kidneys
Results in vasoconstriction, hypertrophy of LV, impaired contractility
243
The early stages of HTN have no signs and is called what?
Lanthanic (silent) dx
244
What are consequences of HTN?
CAD
MI
245
What are coronary heart dx aka CAD result from?
Myocardial ischemia
246
When does CAD produce symptoms?
Until it is fairly advanced because of devleopment of collateral circulation along with plaque
247
What is the leading cause of death among males and females?
CAD
248
What is the patho of CAD?
Diminished coronary perfusion to myocardium relative to myocardium demand
249
What are the risk factors for CAD?
Dyslipidemia
HTN
Smoking
DM and insulin resistance
Obese
Sedentary lifestyle
Atherogenic diet
250
How does dyslipidemia influence plaque development and lead to CAD?
Abnormal concentration in lipoproteins
Increase LDL is strong indication of coronary risk
Low HDL is strong indication of coronary risk
251
How does HTN influence plaque devleopment and cause CAD?
Causes endothelial injury and myocardial hypertrophy which increases myocardial demand
Causes overactivity of SNS and RAAS
252
How does obesity influence plaque devleopment and lead to CAD?
Increased insulin resistance, decreased HDL, increased BP, inflammation
Change adipokines that affect cardiac risk
253
What is metabolic syndrome?
A combination of obesity, dyslipidemia, HTN
254
What does abominal obesity have a strong link to?
Increased CAD risk
255
What are the categories of CAD?
Chronic Ischemic heart Disease (which is stable angina)
Acute coronary syndrome (which is unstable angina and myocardial infarction)
256
What is plaque that is stable and chest pain that subsides with activity?
Stable angina aka angina pectoris
257
What is plaque that is disrupted but stabilizes briefly?
Unstable angina
258
What is plaque disruption that leads to thrombus formation?
Myocardial Infaraction
259
What is the leading cause of death in U.S.
MI
260
What is patho of myocardial infaraction?
1. Sudden change in plaque morphology
2. Plt aggregation & activation and thrombus formation
3. Occlusion of vessel within mins
4. Hypoxic injury and if prolonged necrosis
261
What is the biomarker measured with an heart disease?
Troponin
262
What is the biomarker level with unstable angina?
No increase in level
263
What is the biomarker level with a Non-STEMI?
Increased biomarker level
264
What is the biomarker level with STEMI?
Increased level
265
What are consequences of MI?
Loss of blood supply to myocardium
Arrhythmias
CHF
Cardiogenic shock
266
What does loss of critical blood supply to myocardium with an MI cause?
Hypoxia cell injury
Cell death/necrosis
Decreased function (don’t generate enough pressure)
Consequences of repair
267
What do consequences of repair from an MI result in?
Fibrous scar tissue that lacks:
Contractility
Elastic
Conductive properties
(Can’t handle volume of generate enough pressure)
268
What is sudden death in CHD patients often due to?
V-fib
269
How do arrhythmias occurs?
Ischemia induces heart muscle to become electrically unstable that it failts to contract in coordinated fashion or expel blood from heart
270
What is arrhythmias most likely due to?
Dysregulation of ion balance across cardiomyocyte membrane
271
What are the 3 types of cardiomypathies?
Dilated
Hypertrophic
Restrictive
272
What is the issue with dilated cardiomyopathy (congestive cardiomyopathy)?
Volume issue
LV becomes dilated
273
What are major symptoms of dilated cardiomyopathy?
Fatigue
Weakness
Palpitations
274
What happens to contractility with dilated cardiomyopathy?
Decreased which impairs systolic function
275
What are two types of hypertrophic cardiomyopathy?
Asymmetric sepal hypertrophy
Hypertensive (valvular hypertropic)
276
What is asymmetric septal hypertrophy found in?
Kids who don’t know they have it until drop dead at sporting practice
Inherited heart defect
277
What does asymmetric septal hypertrophy have?
Thicken septal wall that cause outflow obstruction of LVOT
Results in hyperdynamic state with exercise
278
What does hypertensive (valvular hypertropic) cardiomyopathy occur from?
Increased resistance to vent ejection seen in HTN and valvular stenosis
Heart hypertrophy occurs to compensate
279
What is restrictive cardiomyopathy from?
Inability of LV to expand
Muscle losses elsasticity and flexibility
280
What is restricted with restrictive cardiomyopathy?
Filling of vent and reduced diastolic volume of either or both ventricles
Normal systolic function and wall thickness
281
What are disorders of the endocardium?
Valve disorders
Rheumatic heart disease
Infective endocarditis
282
Is infective endocarditis mainly bacterial or viral?
Bacterial
283
What are the 3 hallmarks of infective endocarditis?
Endocardial damage
Bacterial adherence
Formation of vegetation
284
What two factors in involved in patho of heart failure?
Decrease CO and subsuquent decrease in perfusion to other organs like kidneys
Compensatory mechanisms to maintain perfusion
285
How does the compensatory mechanism helps a patient with HF?
They don’t. Makes HF worst
286
What are the compensatory mechanisms of HF that we want to minimize?
Frank Starling
Increased SNS activity
RAAS
Myocardial hypertrophy
287
Are any of the compensatory mechanisms for HF beneficial?
NO
288
What is the frank sterling mechanism and how does it affect HF?
Increase volume will increase stretch which will increase force of contraction
Makes HF worst
289
Is the RAAS system long term or short term? Effect on HF?
Long term by retain Na+ to retain water
Makes HF worst
290
What are the causes of heart failure?
Impaired cardiac function
Excess work demands
291
What are examples of impaired cardiac function that cause HF?
MI
Valvular Dx
292
What are examples of excess work demands that cause heart failure?
HTN
Anemia
Excess fluid administration
293
What is valve stenosis?
Value is narrow and does not open all the way
294
What is valve regurgitation?
Valve does not close all the way
295
What value disorders affect systole?
AV stenosis
MV regurg
296
What valve dirorders affect diastole?
MV stenosis
AV regurg
297
What is congestive heart failure due to?
Failure of heart as a pump with accomplish congestion of body tissues
298
Does congestive heart failure create a pos or neg feedback mechanism?
Pos feedback mechanism that progressively worsens
299
What is the most common mechanical complication of an MI?
Left sided heart failure
300
Mi leads to decreased contractility which does what to the preload and afterload?
Increase both
301
What increases preload due to MI?
Decreased ejection fraction
Increased LVEDV
302
What increases afterload due to MI?
Decreased renal perfusion
Increase renin and angiotensin
303
What does R sided HF cause?
Congestion of peripheral tissue
Dependent edema and ascites and liver congestion
304
What does L side HF cause?
Decreased CO- activity intolerance adn signs of decreased tissue perfusion
Pulmonary congestion-impaired gas exchange and orthopnea
305
What leads to high output failure?
Anemia
Beriberi (Thiamine (B1) deficiency)
Sepsis
Hyperthyroidism (Graves dx)
306
What does shock give rise to?
Systemic hypoperfusion caused by either reduction in CO or in the effective circulating blood volume
307
What are the 4 types of shock?
Cardiogenic
Hypovolemic
Obstructive
Distributive
308
What is hypovolemic shock?
Loss of blood volume, plasma, or ECF
309
What happens to the pressure gradient with hypovolemic shock?
There is no more pressure gradient
It is lost so no blood flow
310
When does hypovolemic shock begin?
When intravascular volume has decreased by about 15%
311
What are the compensatory mechanisms for hypovolemic shock?
Fight or flight response
Redistribute blood from gut and skin to heart and brain
Catecholamine release (increase HR, SVR, contractility)
Shift of interstitial fluid
Adolsteorne, ADH released (retain Na+ so retains water)
Splenic discharge (disgorge stored RBCs
312
What are the main hypoovemic shock compensatory mechanisms?
Increase HR
Vasoconstriction & increased SVR and afterload in order to imporove BP and perfuse vital organs
313
What happens if compensatory mechanisms fail with hypovolemic shock?
Decreased tissue perfusion and cell death
314
What are signs of hypovolemic shock?
High SVR
Rapid HR
Poor skin turgor
Increased thirst
Oliguria
Low systemic and pulmonary preload
Cool, clammy, pale skin
315
What is Cardiogenic shock from?
Inability of heart to pump adequate blood to tissues and end organs
316
What is the most common short term consequence of cardiogenic shock?
Acute MI
Severe episode of MI
317
How is Cardiogenic shock defined?
Persistent HOTN and tissue hypoperfusion caused by cardiac dysfunction in presence of LV failure
318
What are compensatory mechanisms for cardiogenic shock?
SNS Adrenergic (high HR, peripheral vasoconstriction, constrict splanchic to divert blood to heart and brain)
RAAS
Neurohormonal
Which all lead to fluid retention, systemic vasoconstriction, high HR
319
What are hallmark signs of cardiogenic shock?
Tachy
Tachypnea
HOTN
JVD
Dysrthythmias
Low CO
320
What happens with obstructive shock?
inability of heart to fill properly or obstruction to outflow from heart
321
What are examples of obstructive shock?
Cardiac tamponade
Pericardial effusion
PE
Dissected aneurysm
322
What is the issue with obstructive shock?
Restricts volume expansion/preload
323
What is the issue with distributive shock?
Issues is blood vessels and not heart
324
What does distributive shock cause loss of? And examples
Loss of sympathetic motor tone
Anaphylactic
Septic
Neurogenic
325
How does distributive shock effect BP?
Decrease
Cause massive vasodilation
326
How does anaphylactic shock occur?
Widespread hypersensitivity to allergen that triggers an allergic reaction
327
What is released with anaphylactic shock and what does it cause?
Massive histamine release due to inflammatory response
Causes vasodilation
Presence of vasodilators
328
What is septic shock due to?
Presence of inflammatory mediators
Bacterial infection
329
What is the progressive of septic shock?
SIRS, sepsis, severe sepsis, then septic shock
330
What is the compensatory mechanism for septic shock?
Anti-inflammatory response syndrome
331
What are complications of shock?
ARDS (acute respiratory distress syndrome)
Acute renal failure
GI issues
DIC
MODS (multiple organ dysfunction syndrome)
332
What happens to the tissue with septic shock?
Tissue hypoperfusion
333
What is the initial problem with shock?
Decrease tissue perfusion
334
What does decrease tissue perfusion in shock lead to?
Impaired oxygen and glucose delivery which impaired cellular metabolism
335
What 2 things occur with impaired cellular metabolism due to shock?
Impaired oxygen delivery and use
Impaired glucose delivery and use
336
What does impaired oxygen delivery and use lead to with shock?
Anaerobic metabolism which decreases ATP production and increases lactate
337
What type of metabolism does shock become?
Shift to anaerobic metabolism
338
What does impaired glucose delivery and use cause in shock?
Increase serum glucose and release of cathecholamiines, cortisol, GH
339
What does shock cause overall?
Tissue ischemia (inadequate bf) and hypoxia (inadequate oxygen delivery) that leads to acidosis and cell dysfunction
340
How is blood flow affected in hypovolemic and cardiogenic shock?
Bf distribution is reduced to skin, gut, and kidney to maintain blood flow to heart and brain
341
How is blood flow effected with distributive shock?
Bf is unregulated through out skin and organ systems Vasodilation and increased cap permability are present
342
How is cardiac output affected in obstructive shock?
Low CO caused by mechanical issue to bf such as tamponade, tension PTX, PE
343
What is the leading cause of death in first year of life?
Congenital heart defect
344
What are risk factors of congenital heart defects?
Prenatal, environment, genetics
345
What are specific risk factors for congenital heart defects?
Material rubella
Insulin-dependent DM
Alcoholism
Phenylketonuria (PKU)
Hypercalcemia
Drugs
Chromosomal aberrations
346
What are the classifications of congenital heart defects in kids?
Lesions increasing pulmonary bf
Lesions decreasing pulmonary bf
Obstructive lesions
Mixing lesions
347
In congenital heart defects, how do lesions increase pulmonary blood flow and example of it?
Defects that shunt from high pressure left side to low pressure right side with pulmonary congestion; acysnois
Ex: Patent ductus arteriosus
348
What happens in patent ductus arteriosus?
Shunt blood from high pressure left side to low pressure right side causing pulmonary congestion
349
What are the 3 parts of circulation open in fetus?
Ductus venosus
Foramen ovale
Ductus arteriosus
350
What does the 3 holes become when they close when baby takes first breath at birth?
Ductus venosus become ligamentum venosum
Foramen ovale becomes fossa ovalis
Ductus arteriosus becomes ligamentum arteriosus
351
Where is the foramen ovale?
Opening that allows blood to bypass lungs and cross over from RA to LA since fetus lungs are non-functional full of fluid
352
Where is the ductus arteriosus?
Connection between aorta and pulmonary trunk that allows oxygenated blood to bypass fetus nonfunctional lungs since mother supplies oxygenation blood thru placenta for fetus
353
What congenital defects in kids increase pulmonary blood flow?
Patent ductus arteriosus (PDA)
Atria septal defect
Ventricular septal defect
Atrioventricular canal defect
354
What does patent ductus arteriosus lead to?
Increased pulmonary venous return to LA and LV
Increased workload on left side of heart
355
What congenital heart defects in kids decrease pulmonary blood flow?
Tetralogy of fallot (TOF)
Tricuspid Atresia
356
What are the 4 specific defects seen with tetralogy of fallot in kids?
1. Ventricle septal defect high in septum
2. Overriding aorta that straddles VSD
3. Pulmonary valve stenosis
4. RV hypertrophy
357
What is the most common cyanotic congenital heart defect in kids?
Tetralogy of fallot
358
What does tricuspid atresia cause in kids?
Tricuspid valve that has no opening resulting in no way to get blood from RA to RV
359
What do lesions that decrease pulmonary blood flow cause?
A complex right to left shunt and cyanosis
360
What do obstructive lesions cause for congenital heart defects in kids?
Right or left sided outflow tract obstructions that curtail or prohibit blood flow out of heart
No shunting
361
Is there shunting with obstructive lesions that cause congenital heart defects?
NO
362
What are examples of congenital heart defects that cause obstructive lesions?
Contraction of aorta
Hypoplastic left heart syndrome
Aortic/Pulmonary Stenosis
363
What is coarctation of aorta?
Narrowing of lumen of aorta that impedes blood flow
364
What is hypoplastic left heart syndrome?
Underdevelopment of left side heart stuctures
365
What heart structures are underdevelopment in hypoplastic left heart syndrome?
LV
Aorta
Aortic arch
Mitral stenosis
366
What do mixing lesions cause in congenital heart defects in kids?
Desaturated blood and saturated blood mix in chambers or great arteries of heart
367
What are 2 examples of mixing lesions with congenital heart defects in kids?
Transposition of great arteries
Truncus arteriosus
Total Anomalous Pulmonary Venous Connection
368
What is the condition where the aorta arises from the RV and the PA arises from the LV?
Transposition of great arteries
369
What occurs with blood in transposition of great arteries?
Unoxygenated blood circulates continuously thru systemic circulation
Oxygenated blood circulates repeatedly thru pulmonary circulation
370
What is transposition of great arteries incompatible with?
With life unless the 2 pathways have way to communicate
371
What is it called when there is only one main artery arising from both ventricles?
Truncus arteriosus
Failure of large embryonic artery to divide into PA and aorta
372
What are 2 common consequences of congenital heart defects in kids?
Heart failure
Hypoxemia
373
Heart defects that allow desaturated blood to enter systemic systemic without passing thru lungs result in what 2 things?
Hypoxemia
Cyanosis
374
What is it when the arterial oxygen tension is below normal and results in low oxygen artieral saturations?
Hypoxemia
375
What is blue discoloration of mucous membranes and nail ends?
Cyanosis
376
What is cyanosis the result of in kids?
Deoxygenated hemoglobin
377
What are signs of heart failure in kids?
Poor feeding and sucking
Failure to thrive
Dyspnea, tachypnea, diaphoresis, retractions, grunting, nasal flaring wheezing, coughing
Pallor or mottling
Hepatomegaly
Pulmonary overcirculation
378
What is the predominate cause associated with congenital defects in kids?
Pulmonary overcirculation (pressure higher in lungs)
379
What is pulmonary vascular resistance increases that exceed or equal vascular resistance which results in reversal of shunting?
Eisenmenger syndrome
380
What are specific defects in kids that cause hypoxemia and cyanosis?
Lesions that obstruct and shunt from right to left side of heart
Defects involved in mixing saturated and unsaturated blood
Transposition of great arteries
381
What type of hypoxemia is cyanosis only occasionally when stressed in kids?
Mild hypoxemia
382
What type of hypoxemia is feeding intolerance, poor weight gain, tachypnea, and dyspnea seen in kids?
Severe hypoxemia
383
What type of hypoxemia may kids be small for their age and have cognitive/motor skill delays?
Chronic hypoxemia
384
What type of hypoxemia in kids will have polycythemia, SOB with exertion, easily fatigued, exercise intolerance, and clubbing of nail ends?
Chronic hypoxemia
