Patho FINAL

Renal Lab Studies

* GFR
* BUN
* Creatinine
* Clearance rate

Renal Imaging Studies

* IV pyelogram
* renal angiogram
* renal ultrasound

What is Urolithiasis

development of renal calculi (kidney stones) in renal system

Urolithiasis Cause

* urinary stasis
* ↑ urinary levels/level of salts/organic & inorganic acids

Urolithiasis Clinical Mani’s

* PAIN!!!!!
* **Colic:**
* distension of collecting system or ureter
* acute, intermittent, radiating, excruciating
* **Non-Colic:**
* distension of renal calcifies or pelvis
* dull, deep, varying intensities

Urolithiasis Treatment

* pain control
* calculi removal
* prevention (diet w/ food low in Ca+)

What is Acute Tubular Necrosis (ATN)?

* causes damage to internal function of kidney
* impedes blood flow → can lead to acute kidney failure

Pre-renal ATN

occurs when the blood flow to kidney is reduced

Intra-renal ATN

occurs when there is direct damage to kidneys

Post-renal ATN

occurs due to blockage in kidney

What is Polycystic Kidney Disease (PKD)?

growth of fluid-filled cysts bilaterally in kidneys

* cysts replace functional cells (↓ perfusion & obstruction of tubule)
* GENETIC (autosomal dominant)
* non-reversible & cant do anything to make it better

PKD Clinical Mani’s

* enlarged kidney
* HTN
* flank pain
* alt. F & E
* kidney stones
* UTI
* liver/pancreatic cysts
* cardiac valvular disease
* aneurysms

PKD Diagnostics

* family HX
* genetic testing
* Physical
* Imaging

PKD Treatment

* pain control
* treat infection
* BP control
* Dialysis
* renal transplant

Chronic renal failure

kidney holds onto waste

* kidney cant make erythropoietin = NO RBC = NO O2

What is Gastroesophageal Reflux Disease (GERD)

back flow of GI contents into esophagus

What causes GERD?

* fatty foods
* caffeine
* Cigs
* high alcohol intake
* pregnancy
* alteration in anatomy

GERD Complications

* Barret’s Esophagus: happens if disease is untreated
* esophageal mucosal cells undergo metaplasia (pre-cancerous)
* Esophageal Strictures
* Pulmonary Symptoms (cough, asthma, laryngitis)

GERD Nurs. Interventions

* have Pt sit up after eating
* watch Pt for weight loss or changes in voice

What is Peptic Ulcer Disease?

sore that develops on the lining of the esophagus, stomach, or small intestine.

* ranges from slight irritation to ulceration
* PAINFUL AS FUCK!!!!

Peptic Ulcer Disease Causes

* **H. PYLORI! (clearing it promotes ulcer healing)**
* NSAIDS
* Stress
* Smoking
* Genetics
* Pepsin & HCl

Peptic Ulcer Disease Clinical Mani’s

* Gastric

pain occurs on empty stomach OR soon after a meal

Peptic Ulcer Disease Clinical Mani’s

* Duodenal

pain occurs 2-3hrs after a meal & relieved by ingesting more food

Peptic Ulcer Disease Clinical Mani’s

epigastric pain usually relieved by food intake or antacids (esp. dairy)

Peptic Ulcer Disease Complications

* GI bleed/hemorrhage
* erosion into vein/artery (life-threatening)
* Obstruction
* scar tissue interferes w/ passage of GI contents through pylorus
* Perforation
* ulcer erodes through all layers & GI contents enter peritoneum → will cause peritonitis

What is alt. motility?

abnormal nerve/muscle contractions that cause spasms or lack of motion along GI tract

* reduced contraction of hollow structures
* alt. water & vitamin absorption/storage time & risk for obstruction


* diverticular disease also slows motility

What is Hepatocellular Failure?

liver cells DONT WORK

Hepatocellular Failure Clinical Mani’s

* jaundice
* muscle wasting (related to albumin)
* ascites
* impaired protein metabolism
* ↓ albumin (edema) & clotting factors
* impaired absorption of fat-soluable vitamins
* A, D, E, K
* Alt. lipoprotein processing
* abnormal storage of glycogen & release of glucose

Normal Na+ Value

135-145 extra cellular

10-14 intracellular

Normal K+ Value

3\.5-5.0 extracellular

140-150 intracellular

What are Transport Mechanisms?

type of transport based on energy needed

What is Active Transport?

molecules moving against a gradient

* ions going from lower to higher gradient)

What is Passive Transport?

does NOT require energy to move substances across cell membrane

What does the Sodium-Potassium pump do?

moves Na+ & K+ ions against large concentration gradients

What are the 2 compartments of fluid Transport?

* intravascular
* interstitial

What is Intravascular Space?

fluid inside blood vessels

What is Interstitial Space?

fluid found in the spaces around cells

Fluid Transport

* Processes

* **osmosis:** (↑ particles)
* **reabsorption:** (movement of H2O & solutes from the tubule back to plasma)
* **filtration:** (movement of proteins from blood to interstitium)

Fluid Balance: Forces

* Hydrostatic

pressure of fluid

Fluid Balance: Forces

* Osmotic

generated by H2O moving through membrance

Fluid Balance: Regulation

* Thirst
* RAAS system (retention of Na+ & H2O)
* ADH
* Diuretics

Alt. Fluid Balance: Water Content

* hypovolemia s/s

* hemorrhage
* dehydration

Alt. Fluid Balance: Water Content

* hypervolemia s/s

* edema
* water intoxication

What is Cirrhosis?

liver disease characterized by interference of local blood flow & hepatocyte damage

* fluid shifts out = lose intervascular volume
* ↑ hydrostatic pressure
* ↓ colloid osmotic pressure
* ↑ permeability

What is Cirrhosis caused by?

* hepatitis & alcohol abuse
* alt. fluid balance
* portal HTN
* ↓ local blood flow
* hepatocyte damage

Cirrhosis Clinical Mani’s

* ascites
* abd. discomfort
* ↑ girth & weight
* Na+ retention
* hyponatremia
* renal failure (↑ pressure in belly = kidney vasoconstricts = cut down blood flow to kidney = ↓ O2 to organs)

Cirrhosis Diagnosis

* physical exam
* body weight
* abnormal girth

Labs for Cirrhosis

* ascites fluid analysis
* liver & kidney function
* cardiac functions

Cirrhosis Treatment

* paracentesis
* diuresis
* IV albumin (helps fluid stop from shifting)

What is Dehydration?

alterations in F & E electrolyte balance

* Na+ Imbalance
* Negative fluid balance

What causes Dehydration?

* ↓ fluid intake
* ↑ fluid output
* fluid shifts between compartments = ascites

Dehydration Clinical Mani’s

* ↓ LOC
* prolonged cap refill
* ↓/absence of tears
* sunken eyes
* change in vitals
* depressed frontal
* ↓/absent urine output
* ↓ SV, ↓CO, ↑ HR

Dehydration Diagnostic Tests

* HX & Physical
* Characteristics of urine/stool/emesis/sweat
* Nutrition

Labs for Dehydration

blood concentration of:

* electrolytes
* bicarb
* BUN
* Creatinine
* SG

Dehydration Treatment

* Rehydration (oral or IV)
* Correct F & E imbalance

What is Hypoparathyroidism?

Alt. Ca+ balance & negative feedback by parathyroid glands

* body produces parathyroid hormone when Ca+ is low → parathyroid mobilizes Ca+ → as Ca Increases; hormone production stops

Hypoparathyroidism Clinical Mani’s

* hair dryness & loss
* nail breakdown
* skin dryness
* bone loss
* tingling in extremities
* visual changes
* muscle cramps
* seizure
* fatigue

Hypoparathyroidism Diagnostic Tests

* medical & surgical HX
* Physical exam

Labs for Hypoparathyroidism

* parathyroid hormone
* blood Ca+, phosphorus, Mg+
* Urinary Ca+

Hypoparathyroidism Treatment

* Supplementation
* Calcium
* Vitamin D
* Recombinant Parathyroid Hormone

What are the 3 Types of Buffers?

* Plasma: reacts in seconds to hydrogen ion levels
* Respiratory: reacts in minutes to excrete CO2
* Renal: reacts in hrs to days to produce, absorb, & excrete acids/bases/ions

What is Metabolic Acidosis?

HCO3 deficit

Metabolic Acidosis: Contributing Mechanisms

* ↑ production of acid
* ↑ loss of bicarb
* ↑ Cl-
* ↓ secretion of acids by kidney

Metabolic Acidosis Clinical Mani’s

* anorexia
* weakness
* coma
* flushed skin
* nausea/vomiting
* lethargy
* vasodilation
* ↓ HR
* confusion

Metabolic Acidosis Lab Finding

* pH:

What is Metabolic Alkalosis?

↑ in pH caused by plasma excess of HCO3

Metabolic Alkalosis: Contributing Mechanisms

* ↓ in H+ ions
* ↑ HCO3 ions
* loss of Cl- ions

Metabolic Alkalosis Clinical Mani’s

asymptomatic OR s/s related to hypokalemia

* Thready, weak, and irregular pulses
* Muscle weakness
* Nausea/vomiting
* constipation
* abdominal distention

Labs Findings Metabolic Alkalosis

* pH: >7.45
* HCO3: >31

What is insulin required for?

the uptake of glucose by cells

* promotes protein synthesis & formation/storage of lipids
* transport K+, phosphate, Mg+ into cells

Insulin Increases when these increase….

* BG
* amino acids
* K+
* Phosphate
* Mg+
* glucagon
* gastrin

Insulin decreases when these decrease….

* low BG
* high insulin levels
* stimulation of alpha cells

What does the Pancreas produce?

* **endocrine**
* insulin
* glucagon
* **exocrine**
* digestive enzymes
* alkaline fluids
* **islets**
* alpha, beta, and delta cells

What is Diabetes Mellitus?

inability to regulate glucose

* leading to inadequate metabolism of macronutrients

What is Type 1 Diabetes?

absolute or significant deficit of insulin

* cell-mediated immunodestruction of beta cells in pancreas
* Multifactoral: genetic or environmental
* hyperglycemia, hyperketonemia, ketoacidosisTyp

Type 1 Clinical Mani’s

* 3 P’s
* polydipsia- excessive thirst
* polyuria- excessive urination
* polyphagia- excessive hunger
* nocturia
* lethargy
* fatigue
* blurred vision
* weight loss

Type 1 Diagnostic Test

* BG levels
* fasting : >126mg/dL
* random: >200 mg/dL
* prediabetic: 110-125 mg/dL
* urinalysis: ketones, glucose
* HbA1c: ≥ 8%

Type 1 Treatment

* glycemic control (BG 70-120 mg/dL)
* self monitoring & carb intake
* exercise
* insulin replacement therapy

What is Type 2 Diabetes?

insulin resistance & reduction in adequate insulin secretion

* NO destruction of beta cells
* multifactoral
* genetics, obesity, environmental, age >30 yrs, family HX, race

Type 2 Clinical Mani’s

often asymptomatic but s/s may present as

* visual changes
* Coronary artery disease
* Peripheral vascular disease
* recurrent infections
* changes in kidney function
* neuropathy

Type 2 Diagnostic Tests

* HX & Physical
* BG levels

Type 2 Treatment

* weight control
* oral glycemic agents
* insulin replacement
* GOAL: maintain optimal BG levels

Gestational Diabetes

Glucose intolerance w/ onset during pregnancy

* usually temporary but can turn into type 2
* requires diet mods, exercise, and maybe insulin
* IF UNTREATED → can lead to fetal macrosomnia, hypoglycemia, hypocalcemia, & birth defects

Complications of Diabetes

* microvascular

* retinopathy
* nephropathy

Complications of Diabetes

* macrovascular

vascular disease

* coronary artery
* cerebral vascular
* peripheral

Complications of Diabetes

* neuropathy

Nerve degradation

* s/s: numbness, tingling, weakness, pain, muscle wasting

Diabetic ketoacidosis

deficient insulin and severe hyperglycemia

leads to metabolic acidosis

triggered by demand for insulin

kidneys cannot excrete ketones, leads to accumulation of ketones in blood

s/s: consistent with severe hyperglycemia, metabolic acidosis, dehydration

hypoglycemia

low blood sugar

weakness, pallor, cool/clammy skin

\
* Neuroglycopenia symptoms (50 mg/dL or less)
* Glucose deprivation in the brain 
* Headache
* Confusion
* Slurred speech 
* Seizures 
* Coma 
* Death 
* Adrenergic symptoms (55 mg/dL or less) 
* Responses related to the adrenal glands 
* Anxiety 
* Palpitation 
* Tremor 
* Sweating 

hyperglycemia

high blood sugar

* Absence, deficit, resistance of insulin leads to this 
* Significant elevation in blood glucose level 
* Inability to transport glucose and amino acids into cells that require insulin for transport 
* Result of accumulations of circulating blood glucose unmatched by insulin 
* Promotes osmotic diuresis, loss of electrolytes and dehydration 
* Leads to 
* Polyuria 
* Polydipsia 
* Polyphagia 
* Weight loss 
* Weakness 
* Signs of dehydration 
* Leg cramps 
* Poor tissue turgor 
* Cool extremities 
* Tachycardia 

Cardiac connection with Renal System

* The heart's job is to send a continuous supply of oxygenated blood around the body.


* The kidney filters the blood, extracting waste in the form of urine, and also helps regulate the water and salt levels to control blood pressure.

Kidneys & RBC production

kidneys produce a hormone called erythropoietin → which stimulates the bone marrow to make red blood cells needed to carry oxygen (O2) throughout the body.

liver & clotting factors

Bleeding within the body activates a complex system of plasma proteins, called coagulation factors → which promote blood clot formation. 

* The liver is responsible for producing most of these coagulation factors.

Iron Deficiency Anemia

Insufficient iron stores to meet needs for RBC development

What are the major causes of Iron Deficiency Anemia?

* inadequate iron intake
* chronic hemorrhage
* iron malabsorption
* high iron demands

Iron Deficiency Anemia Clinical Mani’s

often asymptomatic

* see s/s
* pallor of the skin and mucous membranes
* fatigue
* weakness
* lightheadedness
* syncope
* headache
* breathlessness
* palpations
* tachycardia
* brittle hails, & mouth sores
* pica

Iron Deficiency Anemia Diagnostics

HX & Physical Exam

Labs:

* H/H
* MCV
* MCHC
* RBC
* Serum ferritin

Iron Deficiency Anemia Treatment

* reverse the cause
* increase iron intake thru diet or supplements

general manifestations of altered urinary elimination

altered volume of excretion

altered excretion characteristics

bleeding

distention

anorexia

pain

vomiting

fever

nausea

general manifestiaons of altered bowel elimination

altered volume and characteristic of stool

bleeding (melena and occult)

pain

abdominal distention

nauseua, pain, vomiting, fever

anorexia

cerebral palsy pathophysiology

cause: event during the antenatal or postnatal periods damaging upper motor neurons

motor dysfunction type: spastic, athetoid/dyskinetic, ataxic

anatomic involvement: hemiplegia, diplegia,quadriplegia