Cardiac & Renal Disorders Flashcards
For every 5 bs of fat you add
2 miles of vessels
Name the 5 vascular layers
E
B
E
S
A
- Endothelium - touching the blood
- Basal lamina
- Elastic lamina
- Smooth muscle - Contract/dilate - Arterioles
- Adventitia - Connective Tissue - Veins
Beta 1 heart receptors
Increases heart rate
Beta 2 heart receptors
Increases contractility and vasodilation
Beta 1 and Beta 2 vascular receptor
Small effect
Alpha 1 vascular receptors
vasoconstriction - norepinephrine
Alpha 2 vascular receptors
vasodilation - epinephrine
What can increase or decrease vascular flow
Vasospasm Inflammation Aneurysm Thrombus Embolus Atherosclerotic plaque
Can you have vasospasm in veins
No only arteries which can result in sudden constriction of smooth muscle and therefore obstruction in flow
Patho of Raynauds Disease
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)
Clin Man of Raynauds Disease
Cold, pale, cyanotic distal fingers numbness or pain
Triggers of Raynauds Disease
Auto-immune diseases, smoking, cold weather, emotional stress, decongestants
Vasculitis
Inflammation of the intima of an artery
Arteritis
Inflammatory in the walls of the artery
AUTOIMMUNE
Buerger Disease Pathophysiology
Inflammatory condition of blood vessels in extremities resulting in micro-thrombus. Caused by SMOKING NOT associated with atherosclerosis (plaque). Men >40
Clinical manifestations of Buerger Disease
Blue = Buerger’s Ischemic pain in the distal vessels Ulcerations and gangrene Phlebitis and venous nodules Diagnosed by biopsy
Temporal Arteritis Pathophysiology
Inflammation of the temporal WITHOUT atherosclerosis
Temporal Arteritis Clinical Manifestations
Unilateral headache on affected side Pain in jaw after chewing FEVER Blurred vision Scalp tenderness
Temporal Arteritis Diagnosis
Elevated sed rate and CRP, CBC may show anemia Biopsy Color flow temporal artery US
Aneurysms
Areas of the arterial wall that balloon outward due to weakening.
Causes of Aneurysms
Atherosclerosis and hypertension are most common cause
True aneurysms vs False aneurysms
True aneurysms affect all three layers of the vessel (saccular and fusiform types) False aneurysms are from vessel damage and blood leakage or dissection
Clinical manifestations of aneurysms
Asymptomatic until rupture often found incidentally
Cerebral Aneurysm vs Aortic aneurysm
Cerebral - increasing ICP - hemorrhagic stroke Aortic - sudden severe tearing pain, radiates into the back/abdomen, shock
2 types of true aneurysms
Saccular and Fusiform
Malignant neoplasms or tumors can result in an embolus due to
Increased coagulation state
How does a pt with arterial vascular obstruction present
Symptoms are below the occlusion, cool and pale below
How does a patient with venous obstruction present
Symptoms are below the occlusion, warm and tender
Thrombus
Happens at the site of damage, Blood clot consisting of platelets, fibrin, erythrocytes, and leukocytes. DVT
Embolus
Thrombus breaks loose and travels through the circulatory system eventually embedding in a smaller vessel. Starts out as DVT then to a Pulmonary Embolus.
Venous thrombosis clinical manifestations
Extremity fullness and edema distal to the thrombus
Arterial thrombosis clinical manifestations
Pallor and coolness extremity distal to the thrombus
6 P’s of acute arterial occlusion
Pallor Paresthesia Paralysis Pain Polar Pulselessness
Lymphedema
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)
Clinical manifestations of lymphedema
Non-pitting, gradual onset, pt c/o heaviness in legs, unilateral or bilateral edema, key is recognizing early
Pathophysiology of Arteriosclerosis
Thickening and hardening of arterial wall due to loss of elasticity and collagen in vessel
ATHerosclerosis
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
Pathophysiology of Atherosclerosis
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
Clinical manifestations of Atherosclerosis
Asymptomatic until at 70% reduction in vessel diameter
Dislipidemia
Total cholesterol >200 Increases the risk of CAD, PAD, Hypertension and Cerebrovascular disease
Primary dyslipidemia vs Secondary dyslipidemia
Primary - Inherited - not related to external factors Secondary - Not inherited - related to environment (diet, obesity, sedentary lifestyle)
VLDL (Triglycerides)
<150
LDL
<100
HDL
40-50
HS-CRP
Shows inflammation in vessels want level <1 if >3 at high risk
Can medications effectively raise HDL
No
Claudication
Pain in legs when walking
Function of the KIDNEY & LIVER
To excrete drugs. So if all drugs use the same excretion system you would not get rid of the drugs effectively
What does the GFR measure
The clearance of a filterable substance from the urine
Look at handout on the RAAS system
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
Micturition
Voiding Involves both reflex and voluntary mechanisms Mediated by the micturition center in the pons
Sympathetic nerves in the bladder
Allow for relaxing and filling of the bladder
Stimulation of the parasympathetic nerves in the bladder
From S2 to S4 parasympathetic nerves result in bladder contraction and relaxation of the internal sphincter to initiate bladder emptying
Urodynamic testing
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
Stress incontinence
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)
Urge incontinence
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
Overflow incontinence
Bladder overflows. Obstruction (narrowing of urethra), large prostate, prolapsed uterus
Mixed Incontinence
Have to ask ?’s several type of disorders
Overactive Bladder
Happens at night too. Increased daytime and nocturnal frequency. The bladder will not relax, always contracting
Functional Incontinence
Related to physical or environmental limitiations. Cannot access the toilet in time. Nothing wrong with the bladder/no access to the bathroom
Transient incontinence
Sudden onset r/t infections, constipation, or impaction. Reversible
Enuresis
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
Neurogenic Bladder
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).
Interstitial Cystitis
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
Bacteriostatic
Prevents bacterial growth
Bacterialcydial
Kills bacterial growth
Nitrates
Infection
Urethral stricture
Blockage in urinary flow partial or complete from the bladder to the urethra
Bladder Cancer
Fifth most common cancer Most tumors originate from the transitional epithelium lining the urinary tract (traditional cell)
Transitional Cell Carcinoma
Bladder cancer hard to treat PAINLESS HEMATURIA
Nephralgia
Renal pain generally at CVA (flank pain)
KUB
Down dirty cheap - shows general size and stones
U/S
Size of a kidney, comparison, always order bilateral (solid tissue or cyst)
CT/MRI
Detailed information about the vascular and tissue in kidneys
IVP
Dye is nephrotoxic have to know renal fx
Renogram
nuclear scan of kidneys which will show vasculature and neoplasms
Hydronephrosis (hydro-water / nephrosis-kidney)
Abnormal dilation of renal pelvis and calyces of one or both kidneys. Colicky intermittent spazmatic pain
Renal agenesis
kidneys do not develop in utero; bilateral - incompatible with life. Can be r/t nephrotoxic drugs
Benign Renal Neoplasm
Nonmetastising growths, cystic No intervention, monitoring
Autosomal Cystic Kidney Disease
Evident at birth; inherited
Kidneys enlarged
Severe systemic HTN (RAAS system)
Liver disease - liver biopsy
Renal Cell Carcinoma
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
Wilms Tumor (nephroblastoma)
Most common CA in children.
Hypertension is a unique sign
Can palpate kidney tumor
Tx Nephrectomy, radiation, chemo
Pyelonephritis
Acute bacterial infection in kidney
WBC’s CASTS Nitrates
Chronic Pyelonephritis
Repeated acute infections Results in loss of nephrons
Nephrolithiasis
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
Benign Prostatic Hyperplasia
Non-malignant enlargement of prostate gland >50 Unknown cause for prostatic stromal cell proliferation (estrogen, delayed apoptosis)
Clinical Manifestations of Benign Prostatic Hyperplasia
LUTS Lower urinary tract symptoms hesitancy, frequency am/pm, reduced stream, post void incontinence Slow onset of sx
Glomerular Structure
3 layers: endothelial lining, basement membrane, epithelial cells
Glomerular Injury
Diffuse >50% Focal <50%
Glomerulonephritis
Inflammatory disorder of the glomeruli
Humoral and cellular
mediated immune response Degradation of the basement membrane results in blood and protein passing
Nephritic Syndrome
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)
Clinical manifestations of Nephritic Syndrome
Tea colored urine Oliguria = Edema = HTN
Glomerulonephritis - Good Pasture Syndrome
Autoimmune IgG Glomerulonephritis with alveolar hemorrhages Rapid & progressive renal failure SOB, hemoptysis due to alveolar hemorrhage
IgA Vasculitis
Children Vasculitis related to immune response HEMATURIA, NO PROTEIN
IgA Nephropathy
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
Nephrotic Syndrome
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
AKI = Acute Kidney Injury
Sudden loss of renal fx
Acute tubular necrosis is most common cause
Prerenal - AKI
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)
Intrarenal - AKI
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
Postrenal AKI
Blocked urine excretion
Acute AKI
Sudden reduction of kidney fx Increased serum CREATINE 1.5x higher than baseline Increased serum creatine results in decreased GFR
AKI RIFLE Classification System
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
First 3 stages of RIFLE system indicate
Severity of disease
Last two-stage of RIFLE system represent
Patient outcomes
R -risk
RIFLE
Increased creatinine x1.5 or GFR decrease >25% UO < 0.5 x6 hours
I - injury
Increased creatinine x2 or GFR decrease >50% UO < 0.5 x12 hours
F - Failure
Increased creatinine x4 or GFR decrease >75% or creatinine >4mg per 100ml UO <0.3 x24 hours or anuria x12 hours
L - Loss
Persistent ARF = complete loss of renal fx >4 weeks
E - ESRD
End Stage Renal Disease
Acute Tubular Necrosis
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
3 Phases of AKI
Prodromal Oliguric Postoliguric
AKI - Prodromal Phase
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
AKI - Oliguric Phase
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
Stages of CKD
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 )
Healthy Vein vs Damaged Vein
2017 Hypertension Guidelines
DASH Diet
Visual effects of Aortic Stenosis
Visual of Mitral Valve Stenosis
Mitral Valve Regurgitation
Clinical Manifestations
Manifestations:
Fatigue
Dizziness
Dyspnea
Palpitations
Leads to left-sided heart failure
Pansystolic (hear it through systole and diastole) high-pitched, blowing murmur
ECG changes with an MI
Sites of ECG changes with MI
Dilated Cardiomyopathy
- 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
Hypertrophic Cardiomyopathy
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
Right Heart Failure
s/s
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
Stages of Heart Failure
FACES
Fatigue
Activity limitations
Congestion
Edema
Shortness of breath
NYHA Heart Failure Classification
Older
Based on symptoms
Definite Symptoms
- Class I - No limitation of physical activity
- Class II - Slight limitation of physical activity, comfortable at rest
- Class III - Marked limitation of physical activity, comfortable at rest
- Class IIIa - no dyspnea at rest Class IIIb - recent dyspnea at rest
- Class IV - Inability to carry on any physical activity without discomfort, symptoms present even at rest
