Case Pres Power Point

8/9/2019 Case Pres Power Point

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Group 6presents

CKD


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Pneumonia, Complicated UTI, Bilateral Ple


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:ISK FACTORSamily HistoryGlucose intoleranceAlcohol Consumption

: > /ender Woman 50 y 0igh Na IntakeSmoking

Sustained in peripheral resistance and blood volume

Stimulates thickening and strengthening of Vessels


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Decrease arterial lumen ,Release of Histamine leukotrines and pros

Injury to the Vessels

vascular permeability

ncrease vascular resistance

Further vessel thickening, , ,Na Ca H2O protein and humoral substance enters cell

HYPERTENSION :BP range140 to 180Over100 to 140

AmlodipineBlopressAngistad

catapres

:NCP Increased BP
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HYPERTENSION

1 converted to A2

lates formation of A1

ACE in the lungs

Renin by the JG apparatusDecrease renal perfusion

Impaired O2 delivery to cells

of Aldosterone by the adrenal glands

Na retention

Potent vasoconstrictor

Chronic Hypertension

Narrowing of the glumerular

arteries

Reduction of glumerular bloo


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Impaired O2 delivery to cells

Decreased GI perfusion

GI ischemia

Decrease GI motility

Constipation Abdominal bloating

Decrease cardiac perfusion

Angina

Lactulosetal stimulation

Dysflatyl

NTG patch( )ISMN Imdur

Decrease renal perfusion

Glumerular ischemia

Glumeruli becomes sclerotic

LUMERULAR NEPHROSCLEROSIS
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rgo vasodilation of the pregulmerular arterioles renal blood flow and glumerular hyperfiltration of the remiaining nephrons workload of the remaining nep

Sclerosis of the remaining nephrons due to overuseProgressive glumerular damage

HRONIC KIDNEY DISEASE: ,DX April 14 2010 lteration in the normal function ofDialysis


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CHRONIC KIDNEY DISEASE

-LOSS OF NON EXCRETORY FUNCTION LOSS OF EXCRETORY FUNCTION

ration in RBC productionVitamin D synthesis impaired

Impaired insulin Alteration in the immune response

Alteration in the regulation of fluid and electrolyteInability to retain albu

Alteration in the excretion of waste productsAlteration in the acid base


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CHRONIC KIDNEY DISEASE

-LOSS OF NON EXCRETORY FUNCTION LOSS OF EXCRETORY FUNCTION

ration in RBC productionVitamin D synthesis impaired

Impaired insulin Alteration in the immune response

Alteration in the regulation of fluid and electrolyteInability to retain albu

Alteration in the excretion of waste productsAlteration in the acid base


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eration in RBC production erythropoeitin production by the kidney ANEMIA

, , HCT HGB RBC HR as compensation

: .abs Apr 23- .Hct 0 31-Hgb 102

- .RBC 3 55

:HR 130

O2 delivery to cells

& :SXFatigueWeakness

DepressionInsomnia cognitive fxn

n of platelet with respect to the vessel wall

Platelet is dispersed

atelet endothelial cell adherance

lity to initiate hemostasis

BLEEDING

/4 16

EPOETIN
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tamin D synthesis impaired Decrease level of Vitamin DDecrease intestinal absorption of calc

HYPOCALCEMIAStimulate parathormone release

( )abs May 5-Ca 2

Caltrate Plus

crease calcium bone resorption

Osteoporosis

Bone fractures
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Defect in the insulin receptors of cells

Impaired insulin action

Erratic blood glucose levels Hyperkalemia

.pr 22-HGT 308

: .abs Apr 24- .K 5 5


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Immune response alteration

UNKNOWN MECHANISM

-Decrease in the number of circulating T B and Natural Killer Lymphocytes

Infection

( . )abs Apr 21- .WBC 18 39

PneumoniaUTI

Ciprofloxacin

ClarithromycinCloxacillin-Pip Tazo

Imepenem

ErythromycinRefrirome

Increase mucus production

ambroxol
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Alteration in the regulation of fluid and electrolyte

Sodium excretion Potassium excretion phosphorus excretion


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Sodium excretion Increase ANP levels Continuous in GFRANP levels cannot co

Sodium retentionHYPERNATREMIA water retentionHYPERTENSION

EDEMACONGESTION

Water from the intracellular goes to ECF

DILUTIONAL HYPONATREMIA

( . )abs Apr 22-Na 124

ThirstFeverry mucous membranerestlessness

RESPERDAL
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Potassium excretion HYPERKALEMIA Ionic imbalance in neuromuscular tissue excitability

Respiratory depression

RESPIRATORY ACIDOSIS

.Muscle weakness including resp muscles

.resp expelling of C02

, - ( - )As pH falls 2 3 diphospoglycerate 2 3 DPG a

:BG Apr 19.O2 74 8Combine with H2O to form carbonic acid

+Release free H and bicarbs ion

Alter Hgb to release O2 and reduces hem

Hgb is strongly alkaline+Resp for picking CO2 and H i

.Resp mechanism failure

bicarbs to buffer free H

+H excreted in form of ammoniu

+H overwhelms compensatory mech

+ +H enter cells and K escapes

Bradycardia

Cardiac arrest

Alteration in cardiac muscle activity

:R 50

Rapid repolarization

:ECG tall and narrow T wave with shortened QT interval

Hyperactive GI

Nausea and vomitingDiarrhea

Intestinal cramping

in the smooth muscle activity

Kalimate
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Phosphorus excretion Hyperphosphatemia Development of phosphate crystalsPruritus

Hypocalcemiad neuromuscular irritability

( )abs May 8- .Ph 1 75

( )abs May 8 .Ca 2 00

Mouth twitchingctive deep tendon reflexes

LaryngospasmSeizures

Tetanytless leg syndrome

Stimulates parathormone release

OsteoporosisBone fracture

calcium influx Arrhythmias


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Inability to retain albumin

Hypoalbuminemia

( . )abs Apr 23- .

Albumin 20 5

Reduction in the intravascular oncotic pressure

Capillary hydrostatic pressure surpasses intravascular oncotic pressureing from the intravascular to intracellular

EdemaCongestion

Accumulation in the pleural space

Pleural effusion

DyspneaTachypnea

Orthopneapen mouth breathingCyanosisxercise intoleranceLethargy

coughALBUMIN with BURINEX
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Alteration in excreting waste product

( )Urea BUN and Creatinine levels

( . )abs Apr 22-Crea 250

- .BUN 15 6

sruption in the neural function Integumentary affectation Gastrointestinal affectation

Cardiovascular affectation Pulmonary affectation Alteration in immune function


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Disruption in the neural function

and demyelinization of nerve fibers

,ing pricking and itching sensation

BUN and Crea accumulation in the brain

Peripheral nerve damage

Restless leg syndrome

Uremic encephalopathy

Reduction in the allertness and awarenessInability to fix attention

Loss of recent memory

Perceptual errors

Deliriumcoma

Motor neuron affectation

Unsteady gait and clumsy with tremulousness

Difficulty performing fine movements of e


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Integumentary affectation

Retention of eurochromes in the skin

:ntegumentary manifestationGray bronze skin color

,Dry flaky skinPruritus

Thin brittle nailsCoarse thinning of hair

Uremic frost

Gastrointestinal affectation

Decomposition of urea in the intestinal flora

:ther GI manifestations( )mmonia odor breath uremic fetorMetalic taste

Mouth ulcerations and bleedingHiccups

Constipation or diarrhealeeding from GI tract

Retention of eurochromes in the skin


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Cardiovascular affectation Pulmonary affectation Alteration in immune function

Extracellular volume expansion.rsecretionof renin asso With HPN

emia increases cardiac work load

Hypertensionitting edemaPeriorbital edema

Pericardial effusionPericardial friction rubEngorged neck veinsHyperkalemia

pericarditis

Crackleshick tenacious sputumDepressed cough reflex

Pleuritic painhortness of breathTachypneaKussmaul type respirationsremic pneumonia

granulocyte countImpair humoral and cell mediated immu

Defective phagocyte function

infection


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Alteration in the acid base balance

+H ion retention

+Accumulation of H ions in the stomach

+ +K H exchange in the linings of the GI with ATPase via active transport

+ -H ion combines with Cl forming HCl acid

Increase HCL acid secretion

Damage to mucosal barrier

in the electric potential across the gastric mucosal memb

+Permit H ion to diffuse int

EPTIC ULCER DISEASE Further damage to the gastr

Neutralization of acid by ammonia

Removal of ammonia via hemodialysis Acidic environment of GI

+Plasma bicarbs and protein binds with excess H ions

cannot be buffered stimulates the chemoreceptorsin the medulla to RR

+partial pressure of arterial Co2 frees H to bind with bicarbs

+neys compensation by secreting excess H onto renal tubulesed by either phosphate or ammonia

Excreted in the urine

F passively diffuses into the cells

y the cells to maintain the balance

HYPERKALEMIA

Decrease albumin synthesisHYPOALBUMINEMIA

( . )abs Apr 23- .Albumin 20 5
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PEPTIC ULCER DISEASE( )Gastic Ulcer

Decrease function of mucosal cells

Decrease quality of mucus

Loss of tight junction between cells

Back diffusion of acid into the gastric mucosa

Further increase acid secretion

Conversion of pepsinogen to pepsin

Further mucosal erosion

Mucosal injury

ucosal erosion reaching the BV of the stomach

.H Pylori

Formation and liberation of histamine

Local vasodilation

Capillary permeabilityLoss of plasma protein

Mucosal edema

Loss of plasma gastric lumen

UPPER GASTROINTESTINAL BLEEDING

MelenaHematemesisccult bleeding

Ischemialuid volume deficit

MucostaRibamipideNexiumOmeprazole

ranexamic acid

Iselpinganaton
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