Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Advanced Pathophysiology > Cardiac & Renal Disorders > Flashcards

Cardiac & Renal Disorders Flashcards

1
Q

For every 5 bs of fat you add

A

2 miles of vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name the 5 vascular layers

E

B

E

S

A

A
  1. Endothelium - touching the blood
  2. Basal lamina
  3. Elastic lamina
  4. Smooth muscle - Contract/dilate - Arterioles
  5. Adventitia - Connective Tissue - Veins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Beta 1 heart receptors

A

Increases heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Beta 2 heart receptors

A

Increases contractility and vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Beta 1 and Beta 2 vascular receptor

A

Small effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Alpha 1 vascular receptors

A

vasoconstriction - norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Alpha 2 vascular receptors

A

vasodilation - epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What can increase or decrease vascular flow

A

Vasospasm Inflammation Aneurysm Thrombus Embolus Atherosclerotic plaque

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Can you have vasospasm in veins

A

No only arteries which can result in sudden constriction of smooth muscle and therefore obstruction in flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Patho of Raynauds Disease

A

PVD not associated with atherosclerosis. Result of vasospasm of small arteries and arterioles. Due to sympathetic stimulation of SNS. W>M. Often associated with another autoimmune disease (SLE, Scleroderma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clin Man of Raynauds Disease

A

Cold, pale, cyanotic distal fingers numbness or pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Triggers of Raynauds Disease

A

Auto-immune diseases, smoking, cold weather, emotional stress, decongestants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Vasculitis

A

Inflammation of the intima of an artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Arteritis

A

Inflammatory in the walls of the artery

AUTOIMMUNE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Buerger Disease Pathophysiology

A

Inflammatory condition of blood vessels in extremities resulting in micro-thrombus. Caused by SMOKING NOT associated with atherosclerosis (plaque). Men >40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinical manifestations of Buerger Disease

A

Blue = Buerger’s Ischemic pain in the distal vessels Ulcerations and gangrene Phlebitis and venous nodules Diagnosed by biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Temporal Arteritis Pathophysiology

A

Inflammation of the temporal WITHOUT atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Temporal Arteritis Clinical Manifestations

A

Unilateral headache on affected side Pain in jaw after chewing FEVER Blurred vision Scalp tenderness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Temporal Arteritis Diagnosis

A

Elevated sed rate and CRP, CBC may show anemia Biopsy Color flow temporal artery US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Aneurysms

A

Areas of the arterial wall that balloon outward due to weakening.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Causes of Aneurysms

A

Atherosclerosis and hypertension are most common cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

True aneurysms vs False aneurysms

A

True aneurysms affect all three layers of the vessel (saccular and fusiform types) False aneurysms are from vessel damage and blood leakage or dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Clinical manifestations of aneurysms

A

Asymptomatic until rupture often found incidentally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Cerebral Aneurysm vs Aortic aneurysm

A

Cerebral - increasing ICP - hemorrhagic stroke Aortic - sudden severe tearing pain, radiates into the back/abdomen, shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

2 types of true aneurysms

A

Saccular and Fusiform

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Malignant neoplasms or tumors can result in an embolus due to

A

Increased coagulation state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does a pt with arterial vascular obstruction present

A

Symptoms are below the occlusion, cool and pale below

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does a patient with venous obstruction present

A

Symptoms are below the occlusion, warm and tender

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Thrombus

A

Happens at the site of damage, Blood clot consisting of platelets, fibrin, erythrocytes, and leukocytes. DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Embolus

A

Thrombus breaks loose and travels through the circulatory system eventually embedding in a smaller vessel. Starts out as DVT then to a Pulmonary Embolus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Venous thrombosis clinical manifestations

A

Extremity fullness and edema distal to the thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Arterial thrombosis clinical manifestations

A

Pallor and coolness extremity distal to the thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

6 P’s of acute arterial occlusion

A

Pallor Paresthesia Paralysis Pain Polar Pulselessness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Lymphedema

A

Swelling due to lymph obstruction. Connected by their own fluid system. Primary is rare r/t congenital abnormality. Secondary is r/t another condition (lymph node resection, radiation, cancer, infection, or injury)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Clinical manifestations of lymphedema

A

Non-pitting, gradual onset, pt c/o heaviness in legs, unilateral or bilateral edema, key is recognizing early

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Pathophysiology of Arteriosclerosis

A

Thickening and hardening of arterial wall due to loss of elasticity and collagen in vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

ATHerosclerosis

A

Type of arteriosclerosis. The buildup of fats and cholesterol to form plaque in the artery wall. Can cause obstruction, decreased tissue perfusion, ischemia and necrosis and can occur in any artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Pathophysiology of Atherosclerosis

A

Accelerated LDL uptake into vessel lining, creation of foam cells, infiltration of macrophages and inflammatory mediators for a chronic inflammatory process, formation of fatty streaks (plaque composed of fibrous cap and fatty streaks) and plaque narrows the vessel lumen causing turbulent flow. Possible rupture and clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Clinical manifestations of Atherosclerosis

A

Asymptomatic until at 70% reduction in vessel diameter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Dislipidemia

A

Total cholesterol >200 Increases the risk of CAD, PAD, Hypertension and Cerebrovascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Primary dyslipidemia vs Secondary dyslipidemia

A

Primary - Inherited - not related to external factors Secondary - Not inherited - related to environment (diet, obesity, sedentary lifestyle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

VLDL (Triglycerides)

A

<150

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

LDL

A

<100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

HDL

A

40-50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

HS-CRP

A

Shows inflammation in vessels want level <1 if >3 at high risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Can medications effectively raise HDL

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Claudication

A

Pain in legs when walking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Function of the KIDNEY & LIVER

A

To excrete drugs. So if all drugs use the same excretion system you would not get rid of the drugs effectively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What does the GFR measure

A

The clearance of a filterable substance from the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Look at handout on the RAAS system

A

There are two ways renin is stimulated: 1. The primary stimulus for secretion is renal hypoperfusion… when renal perfusion is decreased, renin release is stimulated. So, anytime renal blood flow is decreased, renin will be released. The second way… There are specialized cells in the distal tubule that sense Na+ and Cl-. When the concentration of Na+ and Cl- falls renin is released 2. Renin then enters the general circulation acting on angiotensinogen (which is a protein produced in the liver) to convert it to Angiotensin I. 3. Angiotensin I passes through the lung and is converted (by ACE…angiotensin converting enzyme) to Angiotensin II. 4. Angiotensin II is physiologically active and is a potent vasoconstrictor…. Increasing PVR (peripheral vascular resistance) leading to increased BP 5. Angiotensin II also stimulates the adrenal cortex to release aldosterone (a salt-retaining hormone) Aldosterone acts mainly on distal tubule…in the presence of aldosterone Na (and H2O) is reabsorbed and K is secreted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Micturition

A

Voiding Involves both reflex and voluntary mechanisms Mediated by the micturition center in the pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Sympathetic nerves in the bladder

A

Allow for relaxing and filling of the bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Stimulation of the parasympathetic nerves in the bladder

A

From S2 to S4 parasympathetic nerves result in bladder contraction and relaxation of the internal sphincter to initiate bladder emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Urodynamic testing

A

Used for diagnosing voiding dysfx, pt drinks a lot and the bladder is visualized when full, pt voids and the residual amount is then analyzed should be less than 50 - 100ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Stress incontinence

A

Does not happen at night. Occurs when urine is involuntarily lost with increases in intraabdominal pressure (coughing, lifting, sneezing, BM, vomiting, or degenerative neurologic diseases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Urge incontinence

A

Overactive or damaged detrusor muscle! Involuntary sudden leakage of urine along with or immediately following the sensation of a need to urinate. Sudden urge. Secondary to infection, radiation, stones. NO Warning or prompt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Overflow incontinence

A

Bladder overflows. Obstruction (narrowing of urethra), large prostate, prolapsed uterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Mixed Incontinence

A

Have to ask ?’s several type of disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Overactive Bladder

A

Happens at night too. Increased daytime and nocturnal frequency. The bladder will not relax, always contracting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Functional Incontinence

A

Related to physical or environmental limitiations. Cannot access the toilet in time. Nothing wrong with the bladder/no access to the bathroom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Transient incontinence

A

Sudden onset r/t infections, constipation, or impaction. Reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Enuresis

A

Nocturnal overactivity of the detrusor muscle Incontinence while sleeping, common with children Primary - child who has never achieved continence Secondary - develops after a period of at least 6 months of dryness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Neurogenic Bladder

A

Caused by interruption of normal bladder innervation Stroke, Parkinson’s, CP, Spinal Cord injury Manifests as overactive (incontinence) and spastic or inactive and flaccid (retention).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Interstitial Cystitis

A

Chronic bladder pain without apparent cause. Inflammation of the bladder lining, often misdiagnosed as a infection. Have to do cultures to determine inflammation vs. infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Bacteriostatic

A

Prevents bacterial growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Bacterialcydial

A

Kills bacterial growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Nitrates

A

Infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Urethral stricture

A

Blockage in urinary flow partial or complete from the bladder to the urethra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Bladder Cancer

A

Fifth most common cancer Most tumors originate from the transitional epithelium lining the urinary tract (traditional cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Transitional Cell Carcinoma

A

Bladder cancer hard to treat PAINLESS HEMATURIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Nephralgia

A

Renal pain generally at CVA (flank pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

KUB

A

Down dirty cheap - shows general size and stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

U/S

A

Size of a kidney, comparison, always order bilateral (solid tissue or cyst)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

CT/MRI

A

Detailed information about the vascular and tissue in kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

IVP

A

Dye is nephrotoxic have to know renal fx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Renogram

A

nuclear scan of kidneys which will show vasculature and neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Hydronephrosis (hydro-water / nephrosis-kidney)

A

Abnormal dilation of renal pelvis and calyces of one or both kidneys. Colicky intermittent spazmatic pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Renal agenesis

A

kidneys do not develop in utero; bilateral - incompatible with life. Can be r/t nephrotoxic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Benign Renal Neoplasm

A

Nonmetastising growths, cystic No intervention, monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Autosomal Cystic Kidney Disease

A

Evident at birth; inherited

Kidneys enlarged

Severe systemic HTN (RAAS system)

Liver disease - liver biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Renal Cell Carcinoma

A

Renal cell is very curable, the transitional cell is harder to treat Often metastasizes to lung Being obese is an increased risk factor for every type of CA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Wilms Tumor (nephroblastoma)

A

Most common CA in children.

Hypertension is a unique sign

Can palpate kidney tumor

Tx Nephrectomy, radiation, chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Pyelonephritis

A

Acute bacterial infection in kidney

WBC’s CASTS Nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Chronic Pyelonephritis

A

Repeated acute infections Results in loss of nephrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Nephrolithiasis

A

Renal calculi - crystal aggregates composed of organic and inorganic materials within the renal tract Most stones are calcium-based but can be uric acid based

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Benign Prostatic Hyperplasia

A

Non-malignant enlargement of prostate gland >50 Unknown cause for prostatic stromal cell proliferation (estrogen, delayed apoptosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Clinical Manifestations of Benign Prostatic Hyperplasia

A

LUTS Lower urinary tract symptoms hesitancy, frequency am/pm, reduced stream, post void incontinence Slow onset of sx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Glomerular Structure

A

3 layers: endothelial lining, basement membrane, epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Glomerular Injury

A

Diffuse >50% Focal <50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Glomerulonephritis

A

Inflammatory disorder of the glomeruli

Humoral and cellular

mediated immune response Degradation of the basement membrane results in blood and protein passing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Nephritic Syndrome

A

Immune response with inflammation-causing renal capillary damage More common in children Sx present 1-2 weeks after pharyngitis or up to 6 weeks after impetigo (strep throat strep A)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Clinical manifestations of Nephritic Syndrome

A

Tea colored urine Oliguria = Edema = HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Glomerulonephritis - Good Pasture Syndrome

A

Autoimmune IgG Glomerulonephritis with alveolar hemorrhages Rapid & progressive renal failure SOB, hemoptysis due to alveolar hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

IgA Vasculitis

A

Children Vasculitis related to immune response HEMATURIA, NO PROTEIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

IgA Nephropathy

A

Glomerular damage due to IgA protein deposits inside the filters (glomeruli) in the kidneys

Occurs after a URI in adults Hematuria & Proteinuria

Can lead to end-stage renal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Nephrotic Syndrome

A

Immune injury affecting mainly podocytes (barrier to protein passage) Massive amounts of PROTEIN in urine >3.5grms /day Proteinuria leads to hypoalbuminemia and generalized edema (putting out so much protein in urine that it is not staying in vessels since albumin follows fluid the fluid shifts to interstitial = edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

AKI = Acute Kidney Injury

A

Sudden loss of renal fx

Acute tubular necrosis is most common cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Prerenal - AKI

A

Disruption of blood flow to the kidney can be from: Hypotension, renal artery stenosis, dehydration MI, CHF, Diuretics, NSAIDs Prolonged ARF leads to acute tubular necrosis S/S concentrated urine (hanging onto Na+H20 makes serum osmolality high)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Intrarenal - AKI

A

Damage to the structure of the nephrons and kidney Ischemia from renal vein thrombosis, internal vasoconstriction resulting in hypoxia Glomerulonephritis, cast formation in tubules obstructing urine flow Multiple myeloma IV contrast, IV abx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Postrenal AKI

A

Blocked urine excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Acute AKI

A

Sudden reduction of kidney fx Increased serum CREATINE 1.5x higher than baseline Increased serum creatine results in decreased GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

AKI RIFLE Classification System

A

RIFLE criteria

The injury is defined by a doubling of serum creatinine or a reduction of urinary output below 0.5ml/kg per hour during at least 12h.

Patients who develop injury >50% will develop renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

First 3 stages of RIFLE system indicate

A

Severity of disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Last two-stage of RIFLE system represent

A

Patient outcomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

R -risk

RIFLE

A

Increased creatinine x1.5 or GFR decrease >25% UO < 0.5 x6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

I - injury

A

Increased creatinine x2 or GFR decrease >50% UO < 0.5 x12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

F - Failure

A

Increased creatinine x4 or GFR decrease >75% or creatinine >4mg per 100ml UO <0.3 x24 hours or anuria x12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

L - Loss

A

Persistent ARF = complete loss of renal fx >4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

E - ESRD

A

End Stage Renal Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Acute Tubular Necrosis

A

Common cause of AKI Ischemia due to decreased renal perfusion Hypoxia, vasoconstriction, or nephrotoxic medications Results in necrosis of the tubules REVERSIBLE if caught early

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

3 Phases of AKI

A

Prodromal Oliguric Postoliguric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

AKI - Prodromal Phase

A

Early Normal or declining output Serum BUN or creatine begin to rise Insult to kidney has occurred and duration of this phase depends on cause, amt of toxin ingested, duration and severity of hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

AKI - Oliguric Phase

A

May last up to 8 weeks with urine output 50-400ml/day Oliguria and progressive uremia; decreased GFR; hypervolemia Typically lasts 1-2 weeks Dialysis may be required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

AKI - Post Oliguric Phase

A

Renal recovery (5% don’t recover) Urine volume increases May last 1 week with full recovery in 1 year Some degree of renal insufficiency may persist

115
Q

Chronic Kidney Disease

A

Outcome of progressive and irrevocable loss of functional nephrons

Progressive process: CKD then ESRD (requires dialysis) Comorbidities HTN, DM

Decreased kidney fx or kidney damage of 3 months GFR <60 for 3 months with or without indication of damage to kidney

116
Q

Risk factors for Kidney Disease

A

Diabetes HTN Recurrent pyelonephritis Glomerulonephritis Polycystic kidney disease Family history of CKD Hx of exp to toxins >65 YO African American

117
Q

Progression of kidney disease

A

Can lose 75-80% of their nephrons before having issues

118
Q

Stages of CKD

A

STAGE 1 - NORMAL : >90 GFR ( Add 30 to 60)

STAGE 2 - MILD : 60-89 GFR (Add 30)

STAGE 3 - MODERATE : 30-59 GFR (Stage 3 = 30 GFR)

STAGE 4 - SEVERE : 15-45 GFR (Stage 4 - 15)

STAGE 5 = END STAGE : <15 GFR (Stage 5 - 15 )

119
Q

Progression of Chronic Kidney Disease

A

Stages of CKD Focus in stage 1 and 2; minimizing risk factors By stage 3: symptoms may be starting to appear requiring trmt In stage 4: planning for dialysis or transplant should begin In stage 5: transplant or death

120
Q

Complications of Chronic Kidney Disease

A

-Hypertension and cardiovascular disease -Uremic syndrome -Metabolic acidosis

121
Q

Complications of CKD HTN and CVD

A

Hypervolemia, escalated atherosclerotic process, heightened RAAS and SNS activity

122
Q

Complication of CKD Uremic syndrome

A

Retention of metabolic wastes; impaired healing, pruritus; dermatitis, uremic frost

123
Q

Complications of CKD Metabolic acidosis

A

Retention of acidic waste products; hyperkalemia

124
Q

Complications of CKD Electrolyte imbalances

A

Retained K, Phosphorus, Magnesium

125
Q

Complications of CKD Bone and mineral disorders

A

Elevated phosphorus and PTH causes altered bone mineral metabolism; kidneys unable to reabsorb calcium

126
Q

Complications of CKD Malnutrition

A

Decreased intake from uremic syndrome, depression, dietary limitations, changes in taste, protein-energy wasting neg nitrogen balance

127
Q

Complications of CKD Anemia

A

Lack of erythropoietin; uremia shortens RBCs life; combination of worsening CKD, anemia, and heart failure (cardiorenal anemia syndrome)

128
Q

Complications of CKD Depression

A

Comorbid conditions; disease itself ; disruption of social interactions and relationships

129
Q

Peripheral Artery Disease

A

Partial or complete occlusion (stenosis) of the artery resulting in hypoxia to the tissues. Can be slow or fast onset. One or both extremities

130
Q

Risk factors for PAD

A

SMOKING

Age > 70

Diabetes

Dyslipidemia

HTN

131
Q

Clinical Manifestations of PAD

A

Extremity pain with activity with adv disease at rest too

Claudication (intermittent pain with activity)

Pain with elevation of the extremity and improved with dependant position

Dimished pulses

Decreased hair, cooler skin temp

Non-healing ulcers on distal bony area (toes)

Upper extremity - > 15mmHg pressure difference in arms

132
Q

6 P’s of PAD

A
  • PALLOR
  • PULSELESSNESS
  • PARAESTHESIA
  • PARALYSIS
  • POIKILOTHERMIA (COLD)
  • PAIN
133
Q

How does venous blood flow return to the heart

A
  • Veins return blood flow back to the heart through negative thoracic pressure and muscle contraction with physical activity
  • Veins have one-way valves
134
Q

Risk factors for Venous disorders

A

Obesity

Pregnancy

DVT

Liver Disease

Prolonged sitting or standing

135
Q

Explain venous insufficiency

A

Venous valve dysfunctions lead to engorged and enlarged veins usually happens in the legs

Increased hydrostatic venous pressure leads to capillary dilation and increased permeability

Movement of fluid and pigments into the surrounding tissues results in edema and skin discoloration that can lead to tissue necrosis.

remember the veins do not carry clean blood it carries all blood with waste product

136
Q

Healthy Vein vs Damaged Vein

A
137
Q

Clinical Manifestations of Venous Insufficiency

A

Persistent Edema

Heaviness in legs

Rope like varicosities

Stasis pigmentation

Induration

Lipodermatosclerosis

Venous Ulcers ABOVE THE ANKLE

Inflammation may lead to thrombophlebitis

138
Q

Differential Diagnosis for Venous Insufficiency

A

CHF

DVT

Cellulitis

139
Q

How are BP changed mediated

A

Changes in BP are mediated through stimulation of the alpha receptors (epinephrine and norepinephrine) of the sympathetic nervous system (SNS)

Neurotransmitters epinephrine and norepinephrine cause vasoconstriction

140
Q

What does the Parasympathetic Nervous System do with the cardiac system

A

Parasympathetic nervous system stimulation slows the heart rate using the vagus nerve

141
Q

What two things affect BP

A

Cardiac Output (SVxHR)

and systemic vascular resistance

142
Q

Purpose and location of Baroreceptors

A

Baroreceptors are in the aortic arch to detect pressure in the heart and arteries and make adjustments quickly.

143
Q

Purpose of Chemoreceptors

A

Chemoreceptors detect chemical changes in the blood and stimulate the medullary vasomotor center to increase SNS activity

144
Q

Regulation of Systemic Blood Pressure

A

Regulated by neural, hormonal and renal

An increase in ECF volume causes increased CO and SVR to raise BP and causes kidneys to excrete excess sodium and fluid

An increase in serum sodium level causes increased osmolality, increased ADH secretion, and causes the kidneys to reabsorb water

145
Q

BP regulation with the RAAS system

A

Renin-angiotensin-aldosterone system (RAAS) important regulator of BP

  • Low BP stimulates Juxtaglomerular cells to release renin
  • Renin activates angiotensinogen to produce angiotensin I.
  • Angiotensin I contacts with ACE to activate angiotensin II (vasoconstriction)
  • Angiotensin II stimulates release of aldosterone.
  • Aldosterone causes reabsorption of sodium and water passively follows.
146
Q

Nitrous Oxide

A

Potent vasodilator

Vigara

147
Q

Atrial Natriuretic Peptides (ANP)

A

ANP causes kidneys to increase sodium and water excretion by increasing the glomerular filtration rate resulting in urination

If the L/R atrium is stretched (could be volume overload) so the kidneys kick in

148
Q

Endothelin-1

A

Potent vasoconstrictor

149
Q

Circadian Rhythm

A
  • Circadian Rhythm (body’s internal clock) in the brain govern daily variations in bodily functions.
  • Rises before awaking (morning surge)
  • Highest in the middle of the morning
  • Lowest at night (nocturnal dip)
150
Q

Hypertension increases morbidity and mortality associated with

A

Hypertension increases morbidity and mortality associated with heart disease, kidney disease, peripheral vascular disease, and stroke

151
Q

Changes in Hypertension Classification

A

2017 AHA/ACC Guidelines

No more term “Prehypertension”

Stage 1 has been lowered

2 or more NP readings on 2 or more consecutive visits

152
Q

2017 Hypertension Guidelines

A
153
Q

Primary AKA Essential HTN

A

Idiopathic disorder

Most common form of HTN

Rare prior to age 10

Systolic BP major risk factor for cardiovascular disease

154
Q

Primary HTN

Modifiable Risk Factors

A

Dietary factors - Na intake; DASH diet

Sedentary lifestyle

Obesity/weight gain

Metabolic syndrome

Elevated blood glucose levels/diabetes

Elevated total cholesterol

Tobacco

Stress

155
Q

Drug therapy for HTN affects

A

HR

SVR

Stroke volume

156
Q

DASH Diet

A
157
Q

Secondary HTN

A

Hypertension attributed to a specific identifiable pathology or condition.

Infant/Child - most common cause renal disease and coarctation of the aorta and sleep apnea

Adult - r/t renal artery stenosis, pheochromocytoma, pregnancy, obesity/OSA, hyperaldosteronism - most common cause

158
Q

Difference between Hypertensive Emergency and Hypertensive Urgency

A

Hypertensive emergency - sudden increase in S or D BP with end-organ damage

Hypertensive urgency - sudden increase in S or D BP without evidence of end-organ damage

159
Q

Orthostatic (Postural) Hypotension

Criteria

Causes

A

Criteria: Excessive increase in HR (by 20 to 30/BPM)

Dizzyness, blurred vision, confusion, syncope

Assoc with CVD and is a risk factor for stroke, cognitive impairment, and death

Causes: problem with vasomotor or baroreceptor response

adverse drug therapy

arterial stiffness

volume depletion

vasovagal reaction

cardiac dysrhythmias

160
Q

End Diastolic Volume (EDV)

A

Preload (120ml)

Amount returned to the heart between contractions

Ventricular filling pressure prior to contraction

161
Q

Systemic Vascular Resistance (SVR)

A

The resistance to eject blood during a cardiac contraction.

SVR is afterload

SVR is determined by the radius of arteries and degree of a vessel compliance

162
Q

Stroke Volume

A

The amount of blood ejected with each contraction of the ventricle

(S + EDV-ESV)

163
Q

End-systolic volume

ESV

A

Amount of blood that remains in the ventricle after ejection

50ml

164
Q

Ejection Fraction

A

SV/EDV

normal 60-80%

165
Q

Coronary Circulation

Left Main

A

Left main coronary artery divides into left anterior descending and circumflex branches (widow maker)

166
Q

Left Anterior Descending

(LAD)

A

Supplies the septal; anterior, lateral, and apical left ventricle; anterior of the right ventricle

167
Q

Circumflex

A

Supplies the lateral and posterior left ventricles, left atrium

168
Q

Right coronary artery

(RCA)

A

Supplies right atrium, right ventricle, and posterior left ventricle

(SA and AV node)

169
Q

Myocardial ischemia develops with lack of oxygen caused by

A
  • reduced driving pressure
  • reduced vessel diameter
  • reduced perfusion time (due to tachycardia)
  • increased metabolic demand (activity determines)
170
Q

An infarct in the Right Coronary Artery can result in

A

Conduction problems or heart block because of the SA and AV node

171
Q

Cardiac Output

A

The measure of the amount of blood pumped out of the heart each minute

Normal resting is 5-6L

CO = stroke volume X heart rate

172
Q

What determines Cardiac Output

A

The levels of Na, K, and Ca affecting the electrical impulse to initiate contractility.

Availability of ATP (need energy)

Preload

Afterload

173
Q

How does afterload affect cardiac output

A

Afterload is the impedance to ejection from the ventricle and is determined primarily by the aortic blood pressure.

Aortic valve narrowing can significantly increase afterload

  • Increase in afterload increases the ventricular pressure which requires greater tension development within the walls of the chamber (wall stress)
  • Increases myocardial workload
  • Increases oxygen consumption
  • Increases chance of hypertrophy
174
Q

ANP - Atrial Natriuretic Peptide

A

Atrial natriuretic peptide (ANP) synthesized by myocytes and released in response to atrial stretch

ANP and BNP cause enhanced excretion of sodium and water by the kidneys

175
Q

B-type natriuretic peptide (BNP)

A

B-type natriuretic peptide (BNP) produced and released by ventricles in response to chronic overdistention

BNP is elevated in congestive heart failure

176
Q

Automaticity

A

An impulse that cardiac cells initiate to cause contractility

177
Q

Explain the autonomic regulation for rhythmicity of the heart

A

Sympathetic innervation is widespread to all areas of the heart

Parasympathetic innervation via the vagus is localized to the SA and AV nodal areas

Right vagus nerve supplies SA node

Left vagus nerve supplies AV node

178
Q

What takes place during Sympathetic activation

A

Sympathetic activation binds norepinephrine to Beta-1 receptors

Increases heart rate (chronotropic effect)

Increases force of contraction (inotropic effect)

179
Q

Parasympathetic stimulation in the heart

A

Parasympathetic stimulation binds acetylcholine to muscarinic receptors

Reduction in heart rate

Slower speed of action potential conduction

Vasovagal response

180
Q

Action potential

A

Starts at the pacemaker site and spreads throughout the myocardium, electrical current is transmitted to the body surface

Electrical impulse shortens cardiac muscle fibers and causes contraction

181
Q

ECG

A

identifies irregularities in conduction rate or pathways

182
Q

P wave

A

Atrial depolarization - contraction

183
Q

QRS complex

A

Ventricular depolarization - contraction

184
Q

T wave

A

Ventricular repolarization

Recovery

185
Q

U wave

A

in slow heart rate and low potassium

186
Q

Echocardiogram

A
  • Uses ultrasound to provide an image of cardiac structure and motion within the chest
  • Useful in diagnosis of heart enlargement, valvular disorders, collections of fluid in the pericardial space, cardiac tumors, and abnormalities in left ventricular motion
  • Provides estimations of ejection fraction and assessments of ventricular systolic and diastolic function
187
Q

Short PR interval

A

Risk of tachycardia

188
Q

Prolonged QT interval

A

Can cause ventricular arrhythmias

189
Q

What are the two primary pathologic processes in congenital heart anomalies

A
  • Shunting of blood through abnormal pathways in the heart or great vessels
  • Obstruction of blood flow because of abnormal narrowing
190
Q

Heart defects commonly associated with abnormalities in embryologic development

A

Development of the atrial and ventricular septum

Division of the main outflow tract (truncus arteriosus) into the pulmonic and aortic arteries

Development of the valves

191
Q

What is the most common disorder in children and what is it most likely related to?

A
  • Congenital heart disease is the most common heart disorder in children.
  • May be attributed to
  • Maternal rubella during first trimester of pregnancy
  • Exposure to cardiac teratogens
  • Genetic influences
192
Q

Two primary pathologies of Congenital Heart Disease

A

Shunt: abnormal path of blood flow through the heart or great vessels

Right to left: cyanotic (unoxygenated blood going into left side)

Left to right: acyanotic

Obstruction: interference with blood flow because of abnormal narrowing leading to increased workload of affected chamber

Acyanotic

193
Q

Kawasaki Disease

Pathophysiology

A

Systemic vasculitis resulting from infection or toxin stimulus

genetic component

Seen in children under the age of 5

M > F

194
Q

Kawasaki Disease

Clinical Manifestations

A

Fever > 5 days

>101 degrees

Conjunctivitis, oral mucositis with strawberry tongue, truncal rash, erythematous palms and soles, cervical lymphadenopathy

Other manifestations – joint pain, cyanotic extremities

Diagnosis : fever and 4 of the 5 above manifestations

195
Q

Valve Stenosis

A

Failure of a valve to open completely resulting in extra pressure workload for the heart

196
Q

Valve Regurgitation

A

Insufficiency - the inability of a valve to close completely resulting in extra volume workload for the heart

Murmurs result from the abnormal flow through the valve

197
Q

Pericardium

A

The pericardium is the sac that covers the entire heart providing support and protection and maintains the heart in a secure position in the thorax.

Made of collagen and elastin fibers

sac consists of 30 to 40ml of serous fluid

198
Q

Epidemiology of Pericarditis

A
  • Idiopathic
  • Viral infections (cytomegalovirus, coxsackie virus, hepatitis C, IV, flu, Epstein Barr virus)
  • Myocardial Infarction
  • Aortic Dissection
  • Trauma to chest wall
  • Surgery
  • Autoimmune disease (SLE, RA)
  • Metabolic disorders (Uremia)
  • Radiation
  • Chemotherapy
  • Immunosuppressants
  • Causative medications (Hydralazine)
  • Malignancy (breast, lung, lymphoma)
199
Q

Mycarditis

Eitology

A

Inflammation of the mycardium

Infectious

Viral - influenza, CMV, HSV, Adenovirus, Parvovirus

Bacterial - Lyme, mycoplasma

Parasite - Chagas disease

Non-infectious agents - radiation, inf. disorders or sarcoidosis

200
Q

Myocarditis

Clinical Manifestations

A

Clinical manifestations

Asymptomatic or flulike symptoms

Chest pain, palpitations, syncope

Heart failure in severe cases

201
Q

Infective Endocarditis

Eitology

A

Invasion and colonization of the endocardial structures by microorganisms with resulting inflammation.

More common at valvular structures resulting in vegetation growth

Most common bacteria - Staphylococcus or Enterococcus from GI tract

Vegetation breaks loose and becomes emboli

202
Q

Causes of Infective Endocarditis

A

Implanted cardiac devices, invasive procedures, IV drug use

203
Q

Where is the endocardium located

A

Endocardium lines the chamber and it at the valves

204
Q

Infective Endocarditis

Clinical Manifestations

A

Clinical Manifestations:

Fever and chills

Myalgias, arthralgias

New or worsened heart murmur

CHF

Symptoms associated with arterial emboli

205
Q

Rheumatic Heart Disease

A
  • Acute inflammatory disease that follows infection with group A β-hemolytic streptococci
  • Immune attack on connective tissue in joints, heart, skin.
  • Occurs mainly in children – 5-15 yo
  • Fever; sore throat; joint inflammation; a distinctive truncal rash
  • Inflammation causes valve scarring and dysfunction - Mitral and Aortic

Not commonly seen as we use abx to treat strep. The damage can been seen in older adults as a result of this in childhood

206
Q

Aortic Stenosis

Pathophysiology

A

Age-related calcium deposits on the aortic cusps or rheumatic fever

Reduced outflow from the LV into the aorta during systole resulting in decreased cardiac output and LVH develops due to increased workload

Not enough blood going into the systemic circulation with each squeeze. not a big deal at rest but with exertion it is. Coronary arteries is right outside aortic valve if there is a lack of blood flow the coronary arteries will not get what it needs resulting in angina

207
Q

Aortic Stenosis

Clinical Manifestations

RIGHT STERNAL BOARDER MURMUR 2ND INTERCOASTAL SPACE LOUD EASY MURMUR TO HEAR

A

DOE dyspnea on exertion

Fatigue

Angina

Syncope on exertion

Myocardial ischemia and left-sided heart failure

Systolic crescendo decrescendo murmur

Right sternal border 2nd intercostal space very loud murmur

208
Q

Visual effects of Aortic Stenosis

A
209
Q

Aortic Regurgitation

Pathophysiology

A
  • Incompetent aortic valve allows blood to leak back from the aorta into the LV during diastole
  • Increased volume of blood to be pumped out with the next contraction
  • Increased cardiac workload

Valves are loose doesn’t close completely allows blood to flow backward

210
Q

Aortic Regurgitation

Clinical Manifestations

A

Manifestations

  • Fatigue
  • DOE - Dyspnea on EXERTION
  • Angina
  • Syncope
  • Palpitations
  • Leads to LVH and dilation with eventual left-sided HF
  • Diastolic high-pitched blowing murmur - Right sternal boarder 2nd intercoastal space
211
Q

Mitral Valve Stenosis

Patho

A

Reduced outflow from the Left Atrium to the Left Ventricle during Ventricular DIASTOLE

Increased pressure of the LA leads to atrial chamber enlargement and hypertrophy

Cause: calcification or rheumatic fever

212
Q

Mitral Valve Stenosis

Clinical Manifestations

A

Manifestations:

  • Fatigue
  • Palpitations
  • DOE, PND (go to bed normal wake up gasping), Orthopnea •Leads to pulmonary hypertension and eventually RV hypertrophy and right-sided HF - will see sx in lungs sooner due to proximity

Diastolic low-pitched, rumbling murmur

213
Q

Visual of Mitral Valve Stenosis

A
214
Q

Mitral Valve Regurgitation

Patho

A

Incompetent mitral valve allows the backflow of blood from the left ventricle to the left atrium during ventricular systole.

LV and LA both dilate and develop hypertrophy due to extra blood volume

Caused by MI damaging supporting valve tendons damaged chordae tendae

215
Q

Mitral Valve Regurgitation

Clinical Manifestations

A

Manifestations:

Fatigue

Dizziness

Dyspnea

Palpitations

Leads to left-sided heart failure

Pansystolic (hear it through systole and diastole) high-pitched, blowing murmur

216
Q

Mitral Valve Prolapse

Patho

A

Displacement (prolapsing) of the mitral valve leaflets into the left atrium during ventricular systole

W > M

adolescent middle age

Can lead to mitral regurgitation

Clicking pop murmur

217
Q

Mitral Valve Prolapse

Clinical Manifestations

A

Typically asymptomatic

Chest pain

Palpitations

Dyspnea

Can lead to mitral regurgitation

MIDSYSTOLIC click or systolic murmur

218
Q

Coronary Heart Disease

Patho

A

Coronary heart disease (CHD) also called ischemic heart disease and coronary artery disease (CAD)

Characterized by insufficient delivery of oxygenated blood to the myocardium caused by atherosclerotic coronary arteries (CAD)

Risk factors: DM, HTN, Hyperlipidemia, Smoking

219
Q

Vulnerable plaques

A

Vulnerable plaques may rupture or become eroded which stimulates clot formation.

Vulnerable plaques have large lipid core, thin cap, and high shear stress

220
Q

Stable plaques

A

Stable plaques have more collagen and fibrin and a stable cap

221
Q

Coronary perfusion can be altered by

A

Large stable atherosclerotic plaque

acute platelet aggregation and thrombosis

vasospasm

poor perfusion pressure

222
Q

Acute Coronary Syndrome

A

Plaque disruption and thrombus formation and results in unstable angina or MI

Abrupt

Life Threatening

223
Q

Myocardial ischemia may uncommonly be caused by

A
  • coronary vasospasm
  • hypoxemia (high altitude, pulmonary disease)
  • low perfusion pressure from volume depletion or shock
224
Q

Angina Pectoris

A

Chest pain associated with intermittent myocardial ischemia

Ischemia causes a build-up of lactic acid and metabolic wastes in the cardiac tissue causing sx

NO permanent damage occurs

Dx ECG - ST depression

225
Q

3 Patterns of Angina Pectoris

A
  1. Stable or typical angina
  2. Unstable or cresecendo angina
  3. Prinzmental or variant angina
226
Q

Stable or typical angina

A

Most common aka classic

Stenotic atherosclerotic coronary vessels 65-70% narrowing

Predictable onset by similar stimuli

Lasts 3-5 min

227
Q

Unstable or crescendo angina

A

May progress to acute ischemia

Pain occurrence is not predictable

Increasing severity and frequency of sx

228
Q

Prinzmetal or variant angina

A

Unpredictable attacks of anginal pain

Onset of sx is unrelated to physical or emotional exertion, heart rate, or other obvious causes of increased myocardial oxygen demand

Characterized by vasospastic chemicals by local mast cells, and abnormal calcium flux across vascular smooth muscle causing hypercontractility

Minimal to no atherosclerosis

PAIN AT REST OR AT NIGHT

Younger <50 years of age

229
Q

Acute Coronary Syndrome

A

Chest pain >15 min

Plaque rupture with acute thrombus development

Unstable angina - occlusion is partial

MI - occlusion is complete

230
Q

Acute Coronary Syndrome

Diagnosis

Biomarkers

A

ECG - ST elevation

Biomarkers: Myoglobin - elevated at 1 hour, normalizes quickly

CPK-MB - elevates at 4-6 hours

Troponins - develop at 2-6 ours and peaks at 18-24 hours can last 10 days. Doesn’t detect a MI onset less than 6 hours

231
Q

Acute Coronary Syndrome

Clinical Manifestations

A
  • Chest pain >15 min not relieved by rest or nitro
  • Asymptomatic MI : Silent MI
    • Women, the elderly, and patients with diabetic neuropathies
      • Atypical sx, including fatigue, nausea, back pain, and abdominal discomfort
  • ECG changes
    • ST- segment elevation, large Q waves, and inverted T waves
232
Q

STEMI (ST segment elevation)

A

+ Biomarkers

Chest pain with evidence of acute ischemia on ECG

Candidates for acute REPERFUSION therapy

233
Q

NSTEMI (Non-STEMI)

+ Biomarkers

Patients present with symptoms of acute angina and no ST elevation on the ECG

Candidates for ANTIPLATELET drugs

A
234
Q

ECG changes with an MI

A
235
Q

Sites of ECG changes with MI

A
236
Q

Acute occlusion causes a range of cellular events, depending on

A
  • availability and adequacy of collateral blood flow.
  • relative workload
  • length of time that flow is interrupted
237
Q

Prolonged ischemia r/t coronary syndrome leads to

A

Reduced ventricular contractility

Decreased cardiac output

Decreased cardiac output triggers compensatory responses including sympathetic activation

238
Q

Sympathetic nervous system activation leads to myocardial workload by increasing

A

heart rate

contractility

blood pressure

239
Q

Overall prognosis for acute MI affected by:

A
  • How quickly treatment is sought
  • Extent and location of the infarct
  • Previous cardiovascular health
  • Age
  • Presence of other disease processes
240
Q

Cardiac tissue recovery after MI

A

After 18-24 hours area of infarction becomes paler than the surrounding tissue

5-7 days yellowish and soft with rim of red vascular tissue

1-2 weeks necrotic tissue progressively degraded and cleared away

At 1-2 weeks infarcted myocardium weekend and susceptible to rupture

By 6 weeks: Necrotic tissue replaced by tough fibrous scar tissue

241
Q

Cardiomyopathy

Patho

A

Diseases of the heart muscle

Anything that changes the structure or function of the heart

Dilated, hypertrophic, or restrictive types

242
Q

Causes of Cardiomyopathy

A

Primary cause is genetic abnormalities

Secondary Causes

  • Ischemic - CAD
  • Valvular – stenotic or insufficiency
  • Hypertensive – LVH with dilation
  • Inflammatory – myocarditis
243
Q

Dilated Cardiomyopathy

A
  • Dilation of one or both ventricular chambers
  • Slow progression of biventricular heart failure with a reduced ejection fraction

•Systolic dysfunction (cannot squeeze effectively)– dyspnea, orthopnea, exertional intolerance

244
Q

Hypertrophic Cardiomyopathy

A

Thickened so much the LV is tiny

Genetic abnormality

Cause of sudden cardiac death in young patients

NORMAL EJECTION FRACTION

Not a problem with ejection problem with muscle for filling and diastole

245
Q

Restrictive Cardiomyopathy

A

Rarest form of cardiomyopathy

Stiff, fibrotic, rigid, noncompliant ventricle with impaired diastolic filling

Commonly associated with SLE, AMYLOIDOSIS, SARCOIDOSIS, SCLERODERMA (autoimmune)

Affects collagen

Decreased cardiac output and heart failure can result

246
Q

Heart Failure

A

The inability of the heart to maintain sufficient cardiac output to meet metabolic demands of tissues and organs

Problem with impaired contractility

50% die within 5 years of diagnosis

247
Q

Heart Failure Pathogenesis

A

Cause:

  • CAD and HTN - Most common
  • Valvular abnormalities, Sarcoidosis
  • Chemotherapy, appetite suppressants
  • Chronic lung disease

Can be right or left sided or bilateral

LV failure is most common and often leads to RV failure

the worse outcomes are those with low EF

248
Q

Forward heart failure

A

insufficient cardiac pumping manifested by poor cardiac output

249
Q

Backward heart failure

A

Congestion of blood behind the pumping chamber

250
Q

Explain the sympathetic nervous system activation in heart failure

A

Baroreceptor (in carotids and aorta) reflex stimulation due to detecting fall in pressure - increased HR, increased contractility and vasoconstriction (makes the L side of the heart work harder increasing the afterload)

Juxtaglomerular cells release renin, activating the RAAS cascade, resulting in Aldosterone release (increased Na and H20 retention) that increases volume and workload of the heart

These changes result in increased cardiac output temporarily causing increased preload and afterload

Eventually, the myocardial demand cannot be met and the heart decompensates

251
Q

Systolic Dysfx in Heart Failure Patients

A

MI is a common cause of systolic dysfunction - whenever you have a MI you have permanent damage of the heart muscle which prevents it from contracting effectively (systolic/squeeze)

Reduced contractility results in low EF

Loss of cardiac muscle cells and reduced ATP production (no energy for cells to contract.

This is called HFIEF - Heart failure with impaired EF

Low EF <35%

252
Q

Where do you auscultate an aortic murmur

A

Right sternal border 2nd intercoastal space

253
Q

Aortic Stenosis Murmur

A

Right sternal border second intercostal space very loud harsh murmur

254
Q

Aortic Regurgitation Murmur

A

Right sternal border 2nd intercostal space diastolic high pitched blowing murmur

255
Q

Mitral Valve Stenosis Murmur

A

Mid clavicular line 5th intercostal space under breast tissue diastolic low pitched rumbling murmur

256
Q

Diastolic Dysfunction in Heart Failure Patients

A

CAD & HTN main causes

More common in elderly women and those with no history of MI

Disorder of the myocardial relaxation and the ventricle is stiff and does not fill effectively (can’t pump out what you don’t have)

Low cardiac output, vascular congestion, and edema formation with NORMAL EF >40%

HFpEF - Heart failure with preserved EF

257
Q

Left Ventricle Heart Failure

LV damage due to MI or long term HTN

Backward Effects: (what comes before the left ventricle)

A

Accumulation of blood within the pulmonary circulation, pulmonary congestion and eventually edema.

Dyspnea, DOE

Orthopnea (has to sleep with multiple pillows)

Paroxysmal Nocturnal Dyspnea (PND) can fall asleep with 1/2 pillows then wake up gasping when the pulmonary system backs up

Cough, respiratory rales (crackles), hypoxemia and high left atrial pressure, circumoral cyanosis, hemoptyisis

258
Q

Left Ventricle Heart Failure

LV damage due to MI or long term HTN

Forward Effects

A

Results in insufficient cardiac output with decreased oxygenation to peripheral tissues and organs

S3 gallop

Fatigue, weakness, activity intolerance

Tissue hypoxia, renal dysfunction (less blood flow into the kidneys)

259
Q

Right Ventricle Heart Failure

Patho

A

LV heart failure leads to RV heart failure

or

Pulmonary disorders cause increased pulmonary vascular resistance leading to high RV afterload causing right ventricular hypertrophy - caused by issues in the lungs backs up into the RV (cor pulmonale) then RV failure

260
Q

Right Ventricle Heart Failure

Backward effect

A

Caused by congestion in the systemic venous system

Dependant edema, ascites, jugular veins distended (JVD), hepatomegaly, splenomegaly

Hepatogular reflux text; decreased GFR

261
Q

Right Ventricular Heart Failure

Forward effects:

A

Low output to the left ventricle leading to low cardiac output

S4 gallop (blood dropping into a stiff right ventricle)

Fatique and Confusion

262
Q

Right Heart Failure

s/s

A

Right-Sided Heart Failure

  • congestion of peripheral tissues
  • dependant edema and ascites
  • liver congestion - signs related to impaired liver fx
  • Gi tract congestion - Anorexia, GI distress, weight loss
263
Q
A
264
Q

Left-Sided Heart Failure

s/s

A

Left heart failure

  • Decreased cardiac output - act intolerance, s/s decreased tissue perfusion
  • Pulmonary congestion
  • Impaired gas exchange
    • cyanosis and signs of hypoxia
  • Pulmonary edema
    • Orthopnea - has to sleep elevated on pillows
    • Cough with bloody sputum
    • Paroxysmal nocturnal dyspnea
265
Q

Biventricular Heart Failure

A

Most often the result of primary left-sided HF progressing to right-sided HF

Reduced cardiac output

Pulmonary congestion caused by left-sided HF

Systemic venous congestion caused by right-sided

HF

266
Q

HF diagnosis

A

H&P

ECG - LVH, RVH ST depression (heart is being strained)

CXR - pulmonary congestion/effusion

Echo - size of heart chambers, valve abnormalities, EF

Labs: BNP (ventricles dilate), troponins (ischemia), BNP (renal/electrolytes), Thyroid (controls metabolism)

267
Q

Stages of Heart Failure

A

FACES

Fatigue

Activity limitations

Congestion

Edema

Shortness of breath

268
Q

NYHA Heart Failure Classification

Older

Based on symptoms

A

Definite Symptoms

  1. Class I - No limitation of physical activity
  2. Class II - Slight limitation of physical activity, comfortable at rest
  3. Class III - Marked limitation of physical activity, comfortable at rest
    1. Class IIIa - no dyspnea at rest Class IIIb - recent dyspnea at rest
  4. Class IV - Inability to carry on any physical activity without discomfort, symptoms present even at rest
269
Q

ACCF/AHA Heart Failure Classification

Newest

Most associated with the structure of heart

A

ACCF/AHA

  • Stage A - High risk for developing CHF, no structural disorder or the heart (CAD, MI, Diabetics)
  • Stage B - Structural disorder of the heart - Never had symptoms of CHF (Decreased contractility, valve abnormality)
  • Stage C - Past or current symptoms of CHF, symptoms associated with underlying heart disease
  • Stage D - End-stage disease, requires specialized treatment strategies
270
Q
A
271
Q

Chest pain 6 hours possible heart attack or pericarditis. What would you not see is pericarditis

A

A dull pain that improves when you lay down.

Fact: It is a shart pain that improves when you sit up. Patients will tripod

272
Q

High BP 145/102 but patient does not have any other symptoms

A

Hypertension Urgency

273
Q

Patient with heart failure comfortable at rest but dyspneic with walking short distances and a ejection fraction of 30%

A

Because the EF is 30% it is a systolic disfunction b/c the problem is with the “squeeze” of the heart and a 3b the person still has min sx. A person would be a stage C with systolic dysfunction

274
Q

What is NOT a secondary cause of hypertension

a. obesity
b. hypoaldorsterone

A

b. hypoaldosterone

Aldosterone makes you save salt and water which could make you hypertensive. If you are low (hypo) on aldosterone it would not cause htn

275
Q

What stage of renal failure would someone be in with a GFR of 32

A

Stage III

Stage IV is < 30

276
Q

Patient has MI and you see Q wave in V5 and V6 where is the MI

A

Lateral MI

277
Q

Patient has MI and you see Q wave in 1, 2, 3, 4 where is the MI

A

Anterior MI

278
Q

What patient is most likely to have Right-Sided Heart Failure

A

A man with emphysema

It’s the lungs that stress the right side of the heart

279
Q

Left ventricular heart failure does go back into the lungs to cause heart failure

T vs F

A

True

280
Q

True or False

Right-sided HF goes forward to cause HTN

A

False

If you are failing there is not enough blood moving forward to give you HTN

281
Q

Nephrotic Syndrome what will you not see

a. Proteinuria
b. a lot of albumin in vascular system

A

b. albumin is being pushed out in the kidneys so you won’t see it in the vascular system you will have hypoalbuminemia

you will see a lot of Proteinuria over 3grams in Nephritic syndrome you will not see protein in urine

282
Q

Backward effect of left ventricular heart failure

A

backs up into the pulmonary system

283
Q

Pt with HTN what is affecting afterload the most

A

Vascular resistance in the large arteries

Advanced Pathophysiology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions