Hemostasis patho test 4 outline.pdf

Hemostasis

Blood

component

Function Normal

range/

mm3 of

blood

Increase Decrease

Plasma Liquid

portion of

the blood

90% water,

10% solutes-

immune

response,

acid base

balance, and

coagulation

RBC Transports o2

and co2,

contains

hemoglobin

M 4.7-6.1

F 4.2-5.4

X10^6 ul

Congenital heart

disease

Polycythemia vera

Dehydration/

hemoconcentration

Hemorrhage,

hemolysis,

anemia, cancer,

leukemia, renal

failure, over-

hydration, dietary

deficiency

WBC Fight

infection and

react against

foreign

bodies

5,000-

10,000

Infection, trauma, stress,

inflammation

Bone marrow

failure,

overwhelming

infection, drug

toxicity, dietary

deficiency

Platelet Interact with

plasma and

coagulation

factors to

control

bleeding-

contributes

to clotting

150,000-

400,000

Malignant disorder,

polycythemia vera, post-

splenectomy syndrome

Hemorrhage,

hypersplenism,

leukemia,

thrombocytopenia

White Blood Cell Differentials

White blood differential

count

% Absolute

Neutrophils 55-70 2500-8000

Lymphocyte 20-40 1000-4000

Monocytes 2-8 100-700

Eosinophils 1-4 50-500

Basophils 0.5-1 25-100

Hemoglobin (Hgb)

Normal range:

Male- 17.2g/dl female- 15.1g/dl

Increased= polycythemia vera, COPD, dehydration, burns

Decreased= anemia, hemorrhage, cancer, kidney disease

Hematocrit (Hct)

Normal Range:

Male- 40-54% female- 36-48%

Increased= polycythemia vera, dehydration

Decreased= anemia, hemorrhage, bone marrow failure, leukemia

Red Blood Cell Indices

RBC indices Normal range What is it? Increase Decrease

Mean

corpuscular

volume (MCV)

80-95 um^3 Measure if the

average volume

or size of a

single RBC, used

to categorize

anemias

alcoholism,

pernicious

anemia(B12

deficiency), folic

acid deficiency

iron deficiency

anemia,

thalassemia

Mean

Corpuscular

hemoglobin

(MCH)

27-31 pg Measure of the

average amount

(weight) of

hemoglobin

within an RBC

Macrocytic

anemia

Microcytic

anemia

Mean

corpuscular

hemoglobin

concentration

32-36 g/dl or 32-

36%

Measure of the

average

concentration/

percentage of

hemoglobin

Intravascular

hemolysis

Iron deficiency

anemia,

thalassemia

within a single

RBC

Red blood cell

distribution

width (RDW)

11-14.5% Indication of

variations in RBC

size

Iron deficiency

anemias, b12 or

folate deficiency

anemia, sickle

cell disease,

hemolytic

anemias

Anemia

What is it? Cause: Signs and symptoms: Treatment

Nursing

interventions:

condition

marked by

deficiency

of RBCs or

hemoglobi

n in the

blood,

resulting in

pallor and

weakness.

Blood loss

Destructio

n of RBCs

Decreased

or faulty

RBC

productio

1. Impaired o2

transport

Shortness of

breath

Dizziness/

faint

Weakness/

fatigue

Angina

Compensator

mechanism-

tachycardia,

palpations

2. Reduction in red

blood cell indices

and/or Hgb

levels

Decreased

RBC, Hgb,

Hctlab values

Pallor

3. Signs/symptoms

of the process

causing the

anemia

Severity-

acute vs.

Treat the

underlying

cause

Monitor

vitals, input,

and output

Monitor and

control

bleeding

Provide RBC

and fluid

volume

Replacemen

t, plasma

expanders,

colloidal

albumin

chronic

Types of Anemia

1. Blood loss anemia

2. Hemolytic anemia

3. Impaired production of red blood cells

Iron deficiency anemia

Megablastic anemias

Vitamin b12 deficiency

Folic acid deficiency anemia

Aplastic Anemia

Blood loss

anemia

Acute:

Trauma, GI

bleed,

internal loss

Chronic:

May

compensate

over time

Hemolytic Anemia

What is it? Causes: Nursing interventions:

premature

production of

the cell

retention of

iron and other

products of

hemoglobin

destruction in

the body

usually these

are

normochromic

, normocytic

anemias

Intrinsic- defect in the cell

membrane, enzymes

Extrinsic- endotoxins, drugs,

bacterial infection

monitor

---

Impaired production of Red blood cells

Iron deficiency

anemia

Megablastic anemias Aplastic anemia

Causes: Dietary vs. blood

loss

Abnormal nucleic acid

synthesis

results in large RBCs

(floppy) with short

life spans

MCV >100

Deficient nuclear

maturation

Bone marrow depression

Primary: decrease in all

blood cell line

Secondary: chemo,

radiation exposures, viral

hepatitis, mono, other viral

illness

Onset: may be rapid or

slow

signs and

symptoms:

Brittle hair

and nails

Smooth

tongue, oral

ulcers

Pica (craving

non edible

items like

clay, wood,

ice chips)

Treatments: Diet and iron

supplements

Frequent transfusions(replace

RBC,platelets) and bone marrow

transplant

Nursing

interventions:

Monitor

Transfusions

Education

Education,

especially with

pregnancy

Meds

Education: avoid causative

agent

Monitor for infection (often

die from secondary

infections)

Megablastic Anemias Vitamin B12 deficiency

Folic acid deficiency

anemia

Diagnosis:

Shillings test,

B12 serum

levels

Treatment:

Vitamin b12

injections for

life

Diagnosis:

Increased MCV

with normal MCHC

Treatment:

Green leafy veggies,

supplements, fix the

disorder, decrease alcohol

intake

Polycythemia vera

Abnormally high RBC count

Hematocrit greater than 54% in males and 51% in females

Increased WBC and platelet counts

Associated conditions: HTN, venous stasis, HA, stroke

Polycythemia vera- etiology

Relative- decrease in h2o, use of diuretics

Relative to fluid, relatively easy to fix

Primary- proliferation disease of the pluripotent cells of the bone marrow

Too many cells being made and there is no cure

Secondary- physiological increase in RBC production compensatory response to hypoxia-

seen in chronic lung disease patients, CHF, smoking

What Kind of anemia?

Anemia RDW MCV-size used

to classify

anemia

MCH MCHC

Iron deficiency Increase Decreased Decreased Decreased

Vitamin b12 Increase Increased Increased Normal

Folic acid Increase Increased Increased Normal

Hemostasis= prevention of blood loss

Hemostasis-the cascade= the overly, stepwise process for stopping bleeding

5 step process:

Clot dissolution

Clot retraction

Fibrin clot and blood coagulation

Platelet plug

Vessel spasm

Prevention of blood loss step by step

1. Vessel spasm

Reduces blood flow

Prostaglandin, serotonin, endothelin- cause reduced blood flow

The throbbing you feel when you injure yourself

2. Formation of the platelet plug

3. Activating clotting

4. Retraction of clot

Vessel wall edges seal

Activated clotting

Intrinsic pathway- slow process

Extrinsic pathway- faster process

Both interact with calcium ions- conversion of factor x to factor xa

Prothrombin to thrombin

Fibrinogen to fibrin clot

Requirements for the process:

Platelets

Von Willebrand factor

Calcium (factor iv)

Vitamin k- for factor synthesis in the liver

*hemophilia (factor viii and xi) and von Willebrand disease

*vitamin k is necessary for synthesis of factors vii, ix, x prothrombin and protein C. calcium

(factors iv) is required by several step in this process

Clot dissolution-fibrinolysis

Allows blood flow to continue

Controlled by series of activators and inhibitors

-Plasminogen to plasmin

-Breaks down the clot

Requirements for the process:

Platelets

Von Willebrand factor

Calcium (factor ix)

Vitamin k- for factor synthesis in the liver

Lab values and anticoagulants

Prothrombin time (PT) International normalized

ratio (INR)

Partial thromboplastin time

(PTT)

Extrinsic system

Normal range- 11 to

12.5 seconds

Coumadin- to

increase time

Used to calculate therapeutic

levels of coumadin

Intrinsic system

Normal range- 60 to

70 seconds

Heparin

Cardiomyopathies

Cardiomyopathies:

Dilated cardiomyopathies

Hypertrophic cardiomyopathies

Restrictive cardiomyopathies

Rheumatic heart disease:

acute stage –

History of an initiating streptococcal infection

Involves mesenchymal connective tissue of the heart, blood vessels, joints, and subcutaneous

tissues.

R________ phase-

Extension of the cardiac effects of the disease

Chronic phase-

Permanent deformity of the heart valves

Rheumatic Heart disease:

Diagnosis:

Strep testing

EKG changes

Echo changes

Treatment:

Antibiotics

Anti-inflammatory meds

Valve replacement

Function and disorders of heart valves:

Function:

Movement of blood through the chambers of the heart

Dysfunction results in disorders:

Congenital defects

Trauma

Ischemic damage

Degenerative changes

Inflammation

Disruptions occurring with valvular heart disease:

Stenosis-

Narrowing of the valve opening so it does not open properly

Incompetent or regurgitant valve

- Distortion of the valve so it does not close properly

- Permits backward flow to occur when the valve should be closed

Valve disorders:

Mitral valve disorders Aortic valve disorders

Mitral valve stenosis

Mitral valve regurgitation

Mitral valve prolapse

Aortic valve stenosis

Aortic valve regurgitation

Valvular heart disease:

Pg. 562 fig 26-19

Signs and symptoms: shortness of breath, weakness or dizziness, discomfort in chest, swelling in

ankles, feet or abdomen, rapid weight gain

Diagnosis: EKG, echo, chest x-ray

Treatment: percutaneous balloon valvotomy

Renal Function

Terms to know:

Enuresis- the ability to make water and not control it

Glomerular filtration rate- flow rate of filtered fluids that go through the kidney

Loop of henle- segment of the tubule system

Renal clearance – volume that goes through kidneys in one minute

Turbidity- too many particles or too much increase of osmolality

Functions of the kidneys:

Waste processing and elimination

- Na and k ions

- Organic ions (salisalate, penicillin, uric acid, bile acids)

- Urea (protein metabolism product)

- Drugs- those not bound to plasma proteins

Endocrine function

- RAAS

- Erythropoietin

- Vitamin D

Renal blood supply:

Renal artery

2 arterioles

- Afferent and efferent (to/from glomerulus)

2 capillary beds

- Glomerulus- high pressure system

- Peritubular capillary network-low pressure

Peritubular Network:

Low pressure system from the efferent arteriole

Function:

- Convenient for rapid reabsorption of water and solutes (leaving the waste behind)

Parts:

- Peritubular capillaries- surrounds the tubules

- Vasa recta- long, straight, follows loop of henle

Glomerulus:

Glomerulus: high pressure capillary filtration system- between 2 arterioles

high pressure: 2 to 3 times higher than other capillaries

afferent arteriole- from the renal artery

efferent arteriole- to the peritubular capillary vessel

surrounded by thin walled bowman’s capsule

vessels are porous- holes “pores” not so large that blood cells/ plasma proteins can leak

out into the filtrate- gathers in bowman’s capsule

Glomerular Filtration Rate (GFR)

plasma filters into bowman’s space based on:

- capillary filtration pressure

- osmotic pressure

- capillary permeability

filtrate is similar to plasma

- no large proteins

approximately 125 ml/min.

- variable (a few mls to 200 ml/min)

Regulation of renal blood flow:

kidneys receive 20-25% of cardiac output

-goal: maintain GFR to insure waste removal

mechanism

-intrinsic factors- autoregulation, local hormones

-extrinsic factors- SNS, blood borne pathogens

waste removal not perfusion of renal tissue

perfused with 1000-1300ml/minute

regulators keep GFR constant in spite of fluxuations in the arterial pressure

Specific regulation mechanisms:

neural and humoral:

- extrinsic

- SNS

- Angiotension II

- ADH

Auto-regulation- juxtaglomerular complex

- Intrinsic

Dopamine, prostaglandins cause vasodilation- ASA, other Nsaids (prostaglandin

inhibitors) may cause decreased renal blood flow in some cases

Autoregulation mechanism not well understood- JGC suggested

Increased protein in the diet and/or increased glucose levels= increased renal blood

flow= increased GFR= increased urine output

Juxtaglomerular complex- to maintain GFR

Produce and store renin

Feedback control

- Blood pressure

- No levels

Feedback control- links GFR to blood flow/pressure:

-Monitors arterial bp (sensing stretch) in the different arteriole

1. Decreasing bp= release of renin= RAAS stimulation= angiotensin II causes

constriction of efferent arterioles to maintain GFR.

2. Monitors Na levels in the macula densa (to decide how much renin to release to

maintain BP)- angiotension II  aldosterone (function in the kidneys) = na/water

retention to maintain bp

Waste collection- 4 segments of the nephron tubule

Proximal convoluted tubule- a highly coiled segment; drains Bowman’s capsule

Loop of henle- a thin looped structure

Distal convoluted tubule- a distal coiled portion

Collecting tubule- joins with several tubules to collect the filtrate

Tubular function- urine production

Glomerulus produces an ultrafiltrate of urine

Tubules:

- Reabsorb electrolytes, water, nutrients, to maintain homeostasis

- Eliminates waste materials, excess

Movement across membranes require:

Active and passive transport

Na, k, cl, ca, po4 ions

Urate, glucose, amino acids

Concentration gradient

- Water, urea

Endocrine functions of the kidney:

the renin-angiotensin-aldosterone mechanism- RAAS

-plays important part in regulation of blood pressure

Erythropoietin

- Regulates the differentiation of red blood cells in bone marrow

Vitamin D

- Increases calcium absorption from the gastrointestinal

- Helps regulate calcium deposition in bone

Drugs that affect the kidneys:

Diuretics

- Loop : Lasix, demodex

- Thiazide : HCTZ, Maxzide

- Aldosterone : antagonist spironolactone

Action of diuretics:

Loop diuretics Thiazide diuretics The aldosterone antagonists

Exert their effect in thick ascending

loop of henle

Most effective diuretic agents- Lasix

Inhibit the transport system in loop

of henle

Reduce reabsorption of na, k, cl,

and increase elimination of calcium,

magnesium difficult to concentrate

urine (looks like water)

Prevent the

reabsorption of Nacl

in the distal

convoluted tubule

Less effective because

of site of action-

HCTZ, captopril

Potassium wasting

Cause decrease

peripheral vascular

resistance- 1st line

drug for HTN

Reduce sodium reabsorption and

decrease potassium secretion in

the late distal tubule and cortical

collecting tubule site regulated by

aldosterone

(potassium-sparing diuretics)-

spironolactone

Less effective than others

Metabolic acidosis sometimes seen

Testing Renal Functions:

Urinalysis- UA Glomerular filtration rate Blood Urea Nitrogen-

BUN

Creatinine

Clear, amber-colored

fluid

Approximately 95%

water and 5% dissolved

solids

The kidneys normally

produce approximately

1.5L of urine each day

Contains metabolic

wastes and few or no

plasma proteins, blood

cells, or glucose

molecules

Urine osmolarity-

“specific gravity”

1.005 to 1.025

PH- 4.5 to 8, average of 6

Creatinine

-Produce of

creatinine

metabolism in

the muscle

-Filtered by the

kidneys but

not

reabsorbed

Creatinine

clearance used to

measure GFR

- 24 hr. urine

collection

- Two 1 hour

urine

specimens are

collected with

By- product of

protein

metabolism

Eliminated

entirely by the

kidneys

Levels may be

affected by:

-Protein

intake, GI

bleed,

dehydration

2/3rds of renal

function must

be lost before

you see an

increase in BUN

Normal range-

Reflects GFR

Formation and release

is relatively constant

Freely filtered in the

glomeruli

- Not absorbed back

into the blood

- Not much secreted

back into the

tubules

Normal range:

creatine- 0.6 to 1.2

mg/dL

- May need to be

adjusted for age

- Related to loss of

muscle mass and

renal function

blood drawn

in between

8.0 to 20.0

mg/dL

Strong relationship

between renal function

and creatinine level

If creatinine is 2x

normal= loss of ½ renal

function

- 3x normal= loss of

¾ renal function

- Levels at 10mg/dL

or more= loss of

90% of renal

function

Urine abnormals:

Specific gravity high- dehydration

Specific gravity low- decrease renal function (can’t concentrate the urine)

Presence of RBCs, WBCs, bacteria, casts, crystals, protein molecules, glucose, ketones,

etc.

BUN-Creatinine Ratio:

BUN not very specific for renal problems

But when compared with creatinine: Bun creatinine ratio

- >15:1 = pre renal cause of failure- CHF, upper GI bleed

- <10:1 = liver disease, dialysis, low protein diet

Other studies:

Cystoscopy- direct visualization of the internal structures

Ultrasonography- use of high frequency sound waves to visualize deep structures

Radiologic studies- CAT scan, flat plate films, IVP, MRI, radioactive imaging

Tubular components:

Bowman’s capsule

Proximal convoluted tubules

Loop of henle

Distal convoluted tubules

Collecting tubule

Fluid and Electrolyte

Water (fluid) distribution with age

Infants have greater % of body water stored in the interstitial spaces (about 80%);

preemies body weight is about 90% water

Women, obese persons typically have lower water content

Decreases as we get older

- After age 60, water content drops to about 45%

Composition and compartmental Distribution of body fluids

ECF- extra cellular fluid

- Fluid outside of the cell

- Either interstitial (in between tissues)

- Or intravascular (within the vessel)

ICF- intra cellular fluid

- Fluid “within” or inside the cell

ECF and ICF are separated by capillaries and membranes

Electrolytes

Cations (+ charge)

- Sodium

- Potassium

- Calcium

- Magnesium

Anions (- charge)

- Chloride

- Bicarbonate

- Phosphate/phosphorus

Intra CF electrolytes (2+/1-)

Potassium k+

Phosphorus P (aka phosphate)

Magnesium mg+

Extra CF electrolytes (2+/2-)

Sodium Na+

Chloride Cl-

Calcium Ca+

Bicarbonate HCO3-

Sodium 135-145 mEq/L- Main Extra CF cation

Controls body water distribution and governs osmolarity (solute to water ratio)

Controls water distribution by osmosis

Facilitates transmission of nerve and muscle impulses through NA-K pump

Regulation of acid-base balance Na+Cl and bicarbinate (HCO3) changes pH

Ingested in most foods and liquids

IV fluids

Thirst controls water intake (Na+ follows water)

Potassium 3.5-5 mEq/L- main intra CF cation

Helps control ICF osmolarity (concentration of a solution = to the solute to water ratio)

Intake in the diet, need 40 mEq daily- bananas, oranges, strawberries, potato skin

Regulating sodium and water compensatory mechanisms

Decreased Na+ (water gain) serum

osmolality falls thirst diminishes, decrease

in water intake ADH is suppressed renal

excretion increases serum osmolality

normalizes

Increased Na+ (water loss)  rise in serum

osmolality thirst increases, drink more

water ADH release increases renal

excretion decreases serum osmolality

normalizes

Pump it up Na+ and K+

intraCF

-k+ major electrolyte

-fluid within billions of cells in the body (2/3 of fluid)

extra CF

-na+ major electrolyte

-fluid in the interstitial, tissue spaces and blood vessels

-includes plasma

Calcium 8.5-10.5 mg/dL- ECF and ICF cation

major cation in teeth and bones (99%)

found in cell membranes

- help them keep their shape

function:

- increases skeletal muscle contraction

- increases cardiac muscle contraction

- regulates nerve impulse transmissions

- assists in blood clotting

balance:

- role of vitamin D and parathyroid hormone (hypoparathyroidism and

hyperparathyroidism)

intake: dietary

- milk and dairy products- 800 to 1000 mg/day

Magnesium 1.8-3.0 mg/dL

second most plentiful cation in ICF, after K+

stimulates nerve impulse and skeletal muscle contractions

participates in carbohydrate and protein metabolism

activates B complex vitamins and ATP

enhances protein and dna synthesis

facilitates transportation of na and k across cell membranes

influences intracellular Ca through effect on PTH: low Mg impairs action of PTH

Chloride 98-106 mEq/L “The tag along electrolyte”

negatively charged (anion)

assists in the conduction of nerve and muscle transmissions

binds with hydrogen in the stomach to make hydrochloric acid

maintains fluid in blood vessels

Phosphorus 2.5-4.5 mg/dL

largely on ICF anion

incorporated into nucleic acids and ATP

phosphate excess occurs with renal failure and PTH deficit

associated with decreased calcium levels

essential in bone formation

- ingested in diet: milk and meats

metabolic processes- metabolism of fat; glucose, protein

incorporated in cells: dna, rna, and phospholipids layer of cell membrane

serves as acid base buffer in the ECF and in renal excretion of hydrogen ion

needed for normal rbc, wbc and platelet function

Electrolyte balance and movement

electrolytes move fluid in and out of the cell:

- balance is influenced by fluid intake and output

- acid-base balance

- hormone secretion

- normal cell functioning

Imbalance

when cells die due to trauma, chemotherapy, etc…balance is upset

- ICF elctrolytes move out

- ECF electrolytes move in

The body attempts to keep the balance- (homeostasis)

How shall we dance? Said ICF to ECF

Diffusion  ICF leads

Osmosis  ECF leads

Tonicity  whoever is the strongest will lead

Passive transport

Movement of solutes from an area of higher concentration to an area of lower

concentration

Uses the energy created from constant motion of molecules

- The more molecules (concentrated)- the more movement

The purpose is the equalize the concentration in both areas

*diffusion- solutes move, not the fluid

Osmosis

Osmosis is the passage of fluid from an area of high water concentration and less solutes

to an area of higher solutes and comparatively less fluid/water concentration through a

semi permeable membrane (allow some solutes to pass through but not others)

Tonicity

Tonicity: tension or effect that solutes exerts on cell size because of water moving across

the cell membrane

- Isotonic solution

- Hypotonic solution

- Hypertonic solution

Isotonic “the match tonic”

Solute concentration is equal

- Ex: normal saline

- Solution concentration= that of in the blood (unless there is an imbalance)

Hypotonic “lowly tonic”

Solution concentration is lower than normal

- Ex: half normal saline

- Solution and concentration is ½ that of the blood concentration

Hypertonic “over the top tonic”

Solution concentration is greater than another solution

- Ex: 5% dextrose in normal saline

- Solution concentration is greater than that of the blood

Capillary filtration pressure

Results from blood pushing against the walls of the capillary

Interstitial hydrostatic pressure

When the pressure inside a capillary is greater than the pressure in the surrounding

interstitial space, fluids and solutes inside the capillary are forced in the interstitial space

and vice versa

Capillary colloidal osmotic pressure

This process, known as reabsorption, prevents too much fluid from leaving the

capillaries

Albumin acts as a magnet to attract water and hold it outside of the blood vessel

Excess fluid shifts are picked up by the lymphatics and returned to the heart for

circulation

Third space accumulation

When fluid moves out of the intravascular (part of the ECF), but not into the intracellular

space

Results from an increase in permeability of the capillary membrane or a decrease in

plasma colloid osmotic pressure

Fluid re-locates in areas of the body such as:

- Peritoneal cavity-ascites

- Pericardial sac, pleural cavity- effusions

Fluid attributes to weight

- Does not attribute to fulfilling need for fluid or function

Isotonic Fluid volume deficit

Causes: oral trauma, diabetes insipidus

Manifestations: thirsty

Diagnosis and treatment:

Hyponatremia

Sodium (Na) less than <135 mEq/L

Due to decrease or loss of Na

________ Hyponatremia

Osmotic shift from ICF to ECF

- Hyperglycemia: osmotic effect of glucose on the cells

- Na becomes dilute as water moves out of the cells into the ECF- diluting the

concentration of Na

Dilutional Hyponatremia

Water retention

Decrease in Na concentration and tonicity of ECF

Hyponatremia

Condition problem Causes

Hypovolemic Water loss to lesser amount

and Na loss

Diarrhea, vomiting, diuretic

use, sweating

Euvolemic Retention of water/dilution

of Na- normal ECF volume

SIADH or thirst disorder

Hypervolemic High/increased ECF volume Edema forming- CHF,

cirrhosis, kidney disease

Diabetes insipidus

Inability to concentrate urine d/t ADH deficiency or renal insensitivity to ADH

Excessive urine output and thirst

Results in hypertonic dehydration and increased serum osmolality

Urine osmolality= low

Serum osmolality= high

Diagnosis/ management:

Syndrome of inappropriate antidiuretic hormone

Failure of negative feedback system

ADH secretions continue even when serum osmolality is decreased:

- Retention of water more than Na

- Dilutional hyponatremia

Urine osmolality= high

Serum osmolality= low

Cause:

Treatment:

Edema

Increased capillary pressure

Decreased colloidal osmotic pressure

Increased capillary permeability

Obstruction of lymphatic flow

Manifestations of Edema

May be life threatening- brain, lung, larynx

May limit movement

May impede blood flow to muscle or viable tissue- surgical correction may be needed

Pitting edema

Assessment and treatment of Edema

Assessments:

- Daily weights

- Measure girth of effected limb-same location- same time of day each day

- Visual inspection

- Finger pressure to determine if pitting edema- graded 1+ to 4+

Treatment:

- Correct the cause

- Compression

- Elevation

- Diuretics

Trousseau’s sign

Ischemia- induced carpal spasm

- Hypocalcemia

- Hypomagnesemia

Neuromuscular irritability

Occurs during taking bp

Flexion contractor

Chvostek’s sign

Facial irritability

Hypocalcemia

Unilateral spasm induced by tap over the facial nerve CN7

Associated with hypocalcemia

Hypokalemia

Causes: excessive potassium loss in urine due to prescription medications that increase

urination

Manifestations: weakness and fatigue

Treatment: discontinue diuretics

Hyperkalemia

Causes:

Manifestations:

Treatment:

Hypocalcemia

Causes:

Manifestations:

Treatment:

Hypercalcemia

Causes:

Manifestations:

Treatment:

Hypomagnesemia

Causes:

Manifestations:

Treatment:

Hypermagnesemia

Causes:

Manifestations:

Treatment:

Hypophosphatemia

Causes:

Manifestations:

Treatment:

Hyperphosphatemia

Causes:

Manifestations:

Treatment:

Hypochloremia

Causes:

Manifestations:

Treatment:

Hyperchloremia

Causes:

Manifestations:

Treatment:

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