Peptic Ulcer Disease

(what is it/etiologies/types of ulcers with clinical manifestations)

disorders of the upper GI tract caused by the action of acid & pepsin; ulcers are of three locations including the esophagus, stomach, & the duodenum and may be superficial or deep

Etiologies: Helicobacter Pylori, NSAIDs, excessive stress, family Hx (PER JUDY), Smoking, Genetic, Spicy foods & alcohol*

*there is little evidence of a pathogenic role of alcohol & spicy foods

Clinical Manifestations include:

• Gastric Ulcers-
  • heartburn
  • pc(post cibum or consumption) pain
  • food does not relieve pain
• Duodenal Ulcers-
  • Right Epigastric pain that radiates to back
  • food & antacids relieve pain (PER JUDY)
• Other-
  • fullness after eating
  • N/V
  • bloating
  • anorexia
  • wt. loss OR gain
  • hematemesis
  • melena (dark sticky, partly digested feces)

NOTE: PERFORATION & BLEEDING are

MAJOR COMPLICATIONS

Acute & Chronic

Pancreatitis

(what is it/etiologies/pathophys./clinical manifestations/Labs & Tx)

inflammation of the pancreas

Etiologies: biliary obstruction, alcoholism, hypertriglyceridemia, hypercalcemia, infections

Pathophysiology:

• Acute- biliary obstruction → release of enzymes within the pancreatic parenchyma (typically due to obstruction of pancreatic duct) -> enzyme activation -> auto-digestion of pancreas (PER JUDY)
• Chronic- a structural or functional impairment of the pancreas due most often from alcohol abuse

Hepatitis

(what is it/etiologies/clinical manifestations)

inflammation of the liver parenchyma; may be acute or chronic

Etiologies: Hepatitis A, B, C, D, E, CytoMegaloVirus, Epstein-Barr Virus

Clinical Manifestations include:

• Hepatomegaly
• Jaundice
• Light Colored stools
• Skin Rash
• Brown Urine
• Malaise
• Fatigue
• N/V
• HA
• Muscle Aches
• diarrhea
• Electrolyte Imbalances

GastroEsophageal Reflux Disease

(what is it/etiology/clinical manifestations)

backflow of highly acidic gastric contents through the Lower Esophageal Sphincter(LES); can progress to Barretts Esophagus and Esophageal Cancer

Etiology: Any condition or agent that alters the closure strength and efficacy of the LES or ↑ intraabdominal pressure; "weak LES" (PER JUDY)

• Hi Fat Diet
• Hiatal Hernia
• Pregnancy
• Obesity
• Hi Caffeine intake
• Smoking
• Alcohol
• Acidic Foods

Manifestations of

Liver Dysfunction

(5 Categories)

1.) Impaired Protein Sythesis AMB:

• Bleeding- reduced production of bile salts by the liver impairs the absorption of the fat-soluble vitamin K, contributing to poor blood clotting factor production; "Vitamin-K is converted to usable form in the liver" (PER JUDY)
• Edema- inadequate protein metabolism leads to hypoalbuminemia which in turn leads to generalized edema as a result of low serum oncotic pressure
• Immune Deficiency- inadequate protein synthesis leads to decreased substrates for antibody production

NOTE: PORTAL HTN due to the inability of the liver to store blood because of the fatty deposition (cirrhosis). The fat tissue of the liver causes blood to back up into the portal system. (PER JUDY)

Pseudomembranous Enterocolitis

(aka/what is it/predisposing factor/clinical manifestations)

aka Antibiotic-Associated Colitis

an acute inflammation and necrosis of the large intestine caused primarily by CLOSTRIDIUM DIFFICILE, usually affecting the mucosa but sometimes extending to other layers

EXPOSURE TO ABX is the major predisposing factor (PER JUDY)

Clinical Manifestations include:

• diarrhea (often bloody)
• abd. pain
• fever
• perforation (RARE)

Hepatic Encephalopathy is caused by...

HIGH LEVELS of NH₃ (Ammonia) in the blood (PER JUDY) that is not converted to Urea to be passed in the urine due to liver failure/cirrhosis

Esophageal Varices

(what are they/pathogenesis)

distended, tortuous collateral veins that occur from prolonged elevation of pressure; CAUSED BY PORTAL HTN (PER JUDY)

Pathogenesis: Portal HTN → ↑ pressure of collateral veins → swelling of esophageal veins (i.e. varicose veins)

Panic Disorder

(what is it/etiologies/clinical manifestations)

characterized by sudden irrational (FOR NO REASON)fears and acute episodes of severe anxiety 

Etiology: 

• Excess Norepinephrine
• Family H_x
• Substance Abuse
• Major life stress
• Caffeine can be PANICOGENIC (PER JUDY)

Clinical Manifestations include:

• Dyspnea
• Palpitations
• Sense of smothering
• Chest discomfort
• light-headedness
• syncope (fainting)
• diaphoresis (sweating)

Obsessive-Compulsive Disorder

(what is it/obsessions/compulsions)

characterized by persistent involuntary thoughts (OBSESSIONS)that then provoke anxiety and involuntary management rituals (COMPULSIONS)

Obsessions are...

repeated, persistent, unwanted ideas, thoughts, images and have common themes, 

Compulsions are...

repetitive, ritualistic behaviors that prevent or reduce anxiety R/T obsessions, activity (PER JUDY)

NOTE: FAILURE TO PERFORM THE COMPULSIONS CAUSES AN ↑ IN ANXIETY (PER JUDY)

Epidural

hematoma

versus

Subdural

hematoma

Epidural hematoma:

• collection of blood between dura mater & skull
• Typically involves ARTERIAL(PER JUDY)injury and thus RAPID ONSET of S/S
• Usually assoc. with skull fxr; often involves temporal bone with disruption of the middle meningeal artery

Increased IntraCranial Pressure

(what is it/etiology/pathophys./clinical manifestations)

ICP is the pressure exerted by the contents of the cranium and it normally ranges from 0-15 mmHg; volume of cranium is made up of 3 components: BRAIN TISSUE, CSF, & BLOOD. An ↑ in volume of any one of these 3 components will lead to IICP

Etiology: stroke, trauma, tumors, inflammation, hydrocephalus, cerebral edema

• Common Causes include:
  • ↑ Brain Tissue Volume (e.g. tumor)
  • ↑ CSF Volume (e.g. Hydrocephaly)
  • ↑ Blood Volume (e.g. SIADH)

Stroke

(what is it/3 types/etiologies/acute & chronic manifestations)

sudden onset of neurological dysfunction due to cardiovascular disease that results in an area of brain infarction; aka CerebroVascular Accident

1.)Hemorrhagic 

Etiology-> HTN (PER JUDY)

2.)Embolotic

Etiology-> Atrial Fibrillation (PER JUDY)

3.)Thrombotic

Etiology-> Atherosclerosis (PER JUDY)

Acute S/S:

• FOCAL neurological signs(i.e. specific to functions of brain tissue where stroke occurred)

Cerebral Artery-Specific

"Clinical Picture" s/p Stroke

(ACA, MCA, PCA, Vertebral & Basilar)

Anterior Cerebral Artery:

• Contralateral hemiparesis
• Contralateral sensory loss
• Impaired cognition & decision making (PER JUDY)
• Aphasia (LEFT-sided only)
• Incontinence

Errors of Retraction

(4 types)

Myopia: aka Nearsightedness; image focuses in front of retina (PER JUDY)

Hyperopia: aka Farsightedness; image focuses behind the retina (PER JUDY)

Presbyopia: loss of accommodative capacity- inability to see near objects; DUE TO AGING (PER JUDY)

Astigmatism: irregularity in curvature of the cornea (PER JUDY) or lens;

CONDUCTIVE

versus

SENSORINEURAL

Hearing Loss

Conductive Hear loss:

• Disorders of the outer and middle ear whereby sound waves are not reliably conducted to sensory organs of hearing (PER JUDY)
• Recall the Rinnes Test tested Air Conduction to Bone Conduction; in the normal ear, AC>BC
• Causes include: wax(cerumen) ossification of bones (i.e. mallus, incus, stapes), otitis media (i.e.middle ear infections) & edema

Sensorineural Hearing Loss:

• Disorder of the inner ear in the vestibulocochlear apparatus

Merniere Disease

(what is it/pathophys./clinical manifestations)

excessive accumulation of endolymph in the membranous labyrinth (PER JUDY)

Pathophysiology: ↑ volume of endolymph → distention of scala media → membrane ruptures

Clinical Manifestations include:

• Severe rotary vertigo
• Sudden or gradual S/S
• N/Vomiting(PER JUDY)
• Tinnitus(PER JUDY)
• Sensorineural hearing loss
• sense of fullness in ears
• hypotension
• diaphoresis
• nystagmus

Glaucoma

(what is it/pathophys./clinical manifestations)

increased intraocular pressure and progressive loss of vision

Pathophysiology: as fluid pressure inside the eye against the retina increases, blood flow through the retina slows and the retina degenerates and causes a loss of vision

Open-Angle- obstruction impedes the outflow of aqueous humor into the canal of Schlemm → ↑ pressure in the anterior chamber → ↑ pressure in the posterior chamber (MOST COMMON)

Closed-Angle- narrowing of the angle between the pupil & lateral cornea → impaired outflow of aqueous humor (MEDICAL EMERGENCY)

Clinical Manifestations include:

• Open-Angle
  • tunnel vision
  • pain
  • halo
  • blurred vision
  • inability to detect colors
• Closed-Angle
  • sudden severe eye pain (PER JUDY)
  • HA
  • N/V
  • blurred vision
  • halos
  • redness of eye
  • dilated pupil that is unreactive to light
    

Circulatory

"SHOCK"

(what is it/4 types)

inability of the circulation to adequately perfuse the body tissues; imbalance between O2 supply & O2 requirements; occurs first at the cellular level; "HYPOPERFUSION OF TISSUES & DECREASED CARDIAC OUTPUT" (PER JUDY)

4 Types:

1.) Cardiogenic

2.) Hypovolemic

3.) Obstructive

4.) Distributive

-Anaphylactic

-Septic

-Neurogenic

NOTE: ↓ Cardiac Output is the commonality of all categories of shock!

3 Phases of Shock

1.) Compensatory Phase 

• As CO ↓, the compensatory phase involves actions that will counteract the impaired tissue oxygenation
• SNS activation → ↑ HR & Contractility + peripheral vasoconstriction + bronchodilation + ↑ RR
  • this will increase CO and shunt blood from the periphery to the core organs (i.e. brain, heart); this shunting of blood will cause cool clammy skin (PER JUDY)
  • vasoconstriction will ↓ hyrostatic pressure and allow osmotic pressure to prevail causing a fluid reabsorption in the capillaries and thus ↑ preload
  • ↑ RR and bronchodilation will allow for the unloading of CO2 thereby decreasing the mounting acidotic state and promote the oxygenation of as much Hgb as possible
• RAAS → ↑ fluid volume/preload; this will cause the pt. to have ↓ UOP and present with oliguria (PER JUDY)
• ADH Secretion → ↑ fluid volume/preload
• Will continue until problem solves or shock progresses to the next stage
• S/S include:
  • tachycardia (very first sign PER JUDY)
  • ↓ skin perfusion (i.e. CRT>2, pale clammy skin)
  • MS Δ's
  • ↓ UOP/Oliguric
  • dilated pupils

2.) Progressive Phase 

• Compensatory mechanisms can no longer compensate for the  ↓ CO & maintain normal BP
• Prolonged vasoconstriction → progressive tissue hypoxia → Body shifts from aerobic to anaerobic respiration → metabolic acidosis → cell death/lysis
  • as the cells lyse, their contents are released into the interstitium decreasing the circulating volume of ECF due to ↑ osmolarity in the interstitium
• ↓ BP & ↓ CO as precapillary sphincters open due to fatigue/fail over time
• As blood surges into tissue beds, blood flow stagnates → ↑ RISK for DIC
• S/S include:
  • CRT>2
  • Rapid thready pulse
  • Agitation, restlessness, confusion

3.) Irreversible Phase 

• shock is refractory/unyielding to treatment
  
  
  NOTE: COOL CLAMMY SKIN DUE TO THE SHUNTING OF BLOOD TO THE 

Meningitis

(what is it/bacterial vs. viral/clinical manifestations)

inflammation of the meninges (PER JUDY)surrounding the brain and spinal cord; typically complication of open head injuries (PER JUDY)

Viral Meningitis:

• usually self-limiting with complete recovery; pathogen- herpes

Bacterial Meningitis:

• leaves residual effects; pathogens- neisseria meningitidis (PER JUDY), streptococcus pneumoniae, haemophilus influenzae

Alzheimer's Disease

(what is it/pathophys./clinical manifestations)

a progressive neurologic disease of the brain that leads to the irreversible loss of neurons and dementia; dementia is characterized by degeneration of neurons in temporal and frontal lobes

Pathophysiology: unknown trigger → intracellular neurofibrillary tangles + extracellular amyloid plaque → diffuse neuronal damage + brain atrophy (PER JUDY)

NOTE: synthesis of brain neurotransmitter Acetylcholine is deficient and treatment is aimed at increasing ACh levels (PER JUDY)

Clinical Manifestations include: 

• Short-term memory loss
• Decline in cognitive functioning
  • judgement
  • problem solving
  • communication
• Anxiety & Agitation are common
• MRI: brain atrophy & ventricular enlargement
  

Parkinson's Disease

(what is it/pathophys./clinical manifestations)

progressive neurological degeneration disorder; disorder of mobility R/T dopamine deficiency

Pathophysiology: neurons in the basal ganglia/substantia nigra degenerate → ↓ dopamine synthesis → ACh uninhibited causing ↑ muslce excitation

Clinical Manifestations include:

• Tremors (at rest)
• Pill Rolling movements in hands
• Cogwheel rigidity
• loss of facial expression
• drooling
• propulsive gait/impaired balance
• absent arm swing
• orthostatic hypotension
• bradykinesia(PER JUDY)
  
  
  NOTE: PATHOLOGY: "CHANGES IN THE LEVELS OF DOPAMINE" (PER JUDY)
  
  
  
  

Errors of Retraction

(4 types)

Myopia: aka Nearsightedness; image focuses in front of retina (PER JUDY)

Hyperopia: aka Farsightedness; image focuses behind the retina (PER JUDY)

Presbyopia: loss of accommodative capacity- inability to see near objects; DUE TO AGING (PER JUDY)

Astigmatism: irregularity in curvature of the cornea (PER JUDY) or lens;

Pyelonephritis

(what is it/etiology of acute & chronic)

known as infection of the kidney OR upper urinary tract infection; typically involves the renal tubules, parenchyma & the renal pelvis

Etiology of ACUTE Pyelonephritis: ascending (i.e. from the urethra upward) infection whereby the bacteria (e.g. E. COLI) initiate the inflammatory response 

Etiology of CHRONIC Pyelonephritis: recurrent or inadequately managed nonbacterial infections & processes that may be metabolic, chemical, or immunological

 NOTE: clinical manifestations include CostoVertebral Angle pain, & fever

Renal Calculi

(aka/ what are they/etiology/clinical manifestations)

aka- nephrolithiasis OR kidney stones

the presence of a stone or calculus anywhere in the urinary tract; thought to form in the kidneys, tubules, or in the collecting system and then migrate to more distal structures

Etiology: the pathogenesis of nephrolithiasis begins with the urine becoming "supersaturated" with the specific solute; causes of supersaturation include:

• idiopathic hypercalciuria with hyperuricosuria
• hyperparathyroidism
• low urine volume/uop
• abnormal urine pH
• immobility
• excess intake of calcium

Nephrotic Syndrome

(what is it/ patho of edema)

a common set of symptoms caused by damage to the glomeruli, in which proteins cross the glomerulus and are lost in the urine at a rate of >3.5g/day

Patho of Edema: as the serum albumin ↓(HYPOALBUMINEMIA), the osmotic pressure within the blood vessels declines and the hydrostatic pressure is relatively increased, causing a NET flow of fluid into the interstitial spaces

Renal Failure Induced

Anemia

(etiology)

the development of RBCs by the bone marrow depends on numerous cofactors, notably ERYTHROPOIETIN which is produced by the kidneys; AS RENAL FUNCTION ↓, SO TOO DOES THE SECRETION OF ERYTHROPOIETIN

Types of Urinary

Incontinence

(6 types/etiology)

1.) Urge- detrusor overactivity characterized by a strong and immediate urge to void

2.) Stress- caused by increased intra-abdominal pressure; ex. laughing, sneezing

3.) Mixed- a combination of both urge & stress; typically results in greater degree of incontinence and greater disruption with ADLs

4.) Overflow- results from urinary retention and an over distended bladder secondary to obstruction (e.g. BPH) of detrusor under activity

5.) Reflex- urine loss that occurs without sensory warning; neurologic

6.) Functional- result from factors external to the urinary tract; ex. toilet inaccessible, dementia, immobility

Benign Prostatic Hyperplasia

(what is it/clinical manifestations)

a noncancerous enlargement of the prostate gland; prostate increases in size and compresses the urethra and produces symptoms of bladder outlet obstruction

Clinical Manifestations include:

• urinary retention (↑ Post Void Residuals)
• decreased force of stream
• hesitancy
• infection due to residual urine
• nocturia
• dribbling
• urgency
• frequency
• overflow incontinence
• feeling of fullness in the bladder

Urinary Tract Infection

(what is it/etiology/clinical manifestations)

aka cystitis

inflammation of the urothelium (lining of the bladder) resulting from infection, irritation, presence of a foreign body, or trauma

Etiology: Infection (E. COLI), chemical irritants, stones, trauma, sexual activity, catheterization, poor hygiene, urine stasis

Clinical Manifestations include:      

• Dysuria
• + Urine C_x 
• WBC's & RBC's in Urine

Diabetes Mellitus

(what is it/types) 

an endocrine disorder characterized by impaired glucose entry into insulin-sensitive cells due to an absolute or relative deficiency of insulin

Type I (aka Juvenile Onset Diabetes)

VS.

Type II ( aka Adult Onset Diabetes)

**NOTE: HYPERGLYCEMIA will be the presenting** **manifestation of both Type I & Type II DM**

DM Type I

(etiology/pathogenesis/clinical manifestations)

etiology: both idiopathic & immune-mediated=> ZERO insulin production

pathogenesis: Immune-mediated: autoimmune attack on the β-cells of the pancreas -> absolute insulin deficiency -> HYPERGLYCEMIA

Clinical Manifestations include:

• Hyperglycemia (glucagon overproduction causing glycogenolysis & gluconeogenesis)
• Glycosuria (once blood glucose exceeds 320mg/dL which is the T_M for the kidney tubules)
• Polyuria (as osmolarity of urine ↑, the vertical osmotic gradient in the collecting ducts is altered and water reabsorption is less efficient)
• Polydipsia
• Polyphagia
• Weight Loss
• Diabetic KetoAcidosis (MEDICAL EMERGENCY: once ketones present in the urine, pt. must go to E.R. )

DM Type II

(etiology/pathogenesis/clinical manifestations)

Etiology: unknown but biggest risk factor=> OBESITY

Pathogenesis: insulin resistance + Pancreatic β cell dysfunction => relative lack of insulin; + absolute or relative increases in glucagon secretion -> HYPERGLYCEMIA

Clinical Manifestations include:

• Hyperglycemia
• Glycosuria
• Polyuria
• Polydipsia
• Polyphagia
• Hyperglycemic hyperosmolar coma (medical emergency)

NOTE: Ketoacidosis is an uncommon occurrence in Type 2 DM: the presence of endogenous insulin in type 2 DM suppresses the lipolysis that leads to the production of ketone bodies and subsequently ketoacidosis

**NOTE: HYPERGLYCEMIA will be the presenting** **manifestation of both Type I & Type II DM**

Hyperglycemia is...

(clinical manifestations)

an excess of glucose in the bloodstream

Clinical Manifestations include:

• Polyuria
• Polydipsia
• Ketonuria
• Heavy breathing 
• N/V
• Aching, weak, fatigue

Hypoglycemia is...

(clinical manifestations)

deficiency of glucose in the bloodstream

Clinical Manifestations include:

• Cold Sweats
• HA
• Trembling
• Pounding Heart
• Sleepiness
• Personality Change
• Hunger

Vascular Complications

Chronic Hyperglycemia

(Microvascular & Macrovascular)

Microvascular Complications:  

• Retinopathy
• Nephropathy

Neuropathic Complications

of Chronic Hyperglycemia

(autonomic & sensory dysfunction)

NEUROPATHY is manifested by PAIN &

LOSS of FUNCTION; responsible for ↑serious foot problems (i.e. PVD -> ischemia -> amputation)

Autonomic Dysfunction:

• GI disturbances - gastroparesis, diabetic diarrhea, fecal incontinence
• Bladder dysfunction -neurogenic bladder
• Cardiovascular -tachycardia, orthostatic hypotension
• Sexual Dysfunction -erectile dysfunction

Erectile Dysfunction

(what is it/etiology/risk factors)

aka "Impotence"

failure to achieve and maintain an erection of the penis

Etiology: 

Primary: an inability to attain an erection throughout life; often due to deep-seated psychiatric problems

Secondary: PVD, iatrogenic, endocrine disorders, trauma, psychological

Risk Factors: 

• Diabetes
• HTN
• PVD

Dysmenorrhea is...

(definition/etiology)

menstruation that is painful enough to limit normal activity or to cause a woman to seek health care

Etiology: PROSTAGLANDINS!!!!! Under the influence of progesterone, the endometrium releases prostaglandins. Prostaglandins have significant effects on smooth muscle & vasomotor tone promoting uterine contractions and ischemia of the endometrial capillaries and thereby cause the cramping pain of dysmenorrhea.

Rectocele

VS.

Cystocele

Rectocele: aka Protocele; a protrusion of the anterior rectal wall into the posterior of the vagina at a weakened part of the vaginal musculature

Clinical Manifestations include:  

• constipation
• painful BM
• dyspareunia (i.e. painful intercourse)

Endometriosis 

(what is it/etiology/clinical manifestations)

growth of endometrial tissue that grows outside the lining of the uterine cavity; endometrial tissue outside the uterus responds to hormones (i.e. estrogen & progesterone) causing build up, scarring, and further growth

Etiology: THEORIES include Transportation, Metaplasia, & Induction. In class we focus on the Transportation theory that contends  that endometrial tissue flows backward through the oviducts during a normal menstrual period and implant on the ovary, peritoneal surfaces, and other areas

Clinical Manifestations include:

• acquired dysmenorrhea (pain  in the lower part of the abd, vagina, posterior of the pelvis, and back

Glomerulonephritis

(causative organism)

β hemolytic streptococcus

Acute & Chronic

Pancreatitis

(what is it/etiologies/pathophys./clinical manifestations/Labs & Tx)

inflammation of the pancreas

Etiologies: biliary obstruction, alcoholism, hypertriglyceridemia, hypercalcemia, infections

Pathophysiology:

• Acute- biliary obstruction → release of enzymes within the pancreatic parenchyma (typically due to obstruction of pancreatic duct) -> enzyme activation -> auto-digestion of pancreas (PER JUDY)
• Chronic- a structural or functional impairment of the pancreas due most often from alcohol abuse

Types of

Intestinal Obstruction

(what is it/types)

inability of the intestinal contents to progress through the bowel

1.) Mechanical Obstruction: caused by condition that decrease the patency of the bowel.

• Intussusception
• Volvulus

NOTE: "CLINICAL MANIFESTATIONS of BOWEL OBSTRUCTIONS due to accumulation of whatever proximal to the obstruction" (PER JUDY)

Intestinal Obstructions

(etiologies/pathophys./clinical manifestations)

Etiologies: intestinal adhesions, hernias, tumors, severe constipation, surgery, prolonged bedrest

Pathophysiology: Obstruction of intestinal lumen -> abd. distention of gas & fluids proximal to obstruction -> ↓ absorption of water & electrolytes + Vomiting -> Hypovolemia + Dehydration -> impaired blood supply -> ISCHEMIA -> Necrosis -> leakage of intestinal contents into peritoneum -> bacteremia -> possible SEPSIS

Clinical Manifestations include:

• colicky pain
• abd. distention
• hypoactive bowel sounds distal to obstruction/hyperactive bowel sounds proximal to obstruction
• N/V 
• Anorexia
• Diarrhea
• Abd. tenderness
• electrolyte imbalances

Seizures & Epilepsy

(what are they/etiology/pathophys./clinical manifestations)

Seizure- a transient neurologic event of paroxysmal abnormal or excessive cortical electrical discharges that is manifested by disturbances of skeletal motor function, sensation, autonomic visceral function, behavior, or consciousness

Epilepsy- group of disorders characterized by recurrent seizures

Etiology:

• Head Injury
• Infections
• Space-Occupying Lesions
• Metabolic- electrolyte imbalance, hypoxia, acidosis, renal failure
• drugs
• genetic
• acquired from pathologic conditions

Septic Shock

(what is it/etiology/pathophys./clinical manifestations)

results from severe systemic inflammatory response to infection; MOST COMMON μ-organism E.COLI;

Etiology: Bacteremia

Pathophysiology: Bacteremia (i.e. bacteria in blood) → septicemia (endo/exotoxins in blood) →  systemic inflammatory response + complement activation + clotting cascade activation + kinin system activation → misdistribution of blood flow

NOTE: ENDO/EXOTOXINS cause  massive VASODILATION (PER JUDY)

Clinical Manifestations include:

• Normotensive
• Hyperthermia/FEVER (i.e. 104°F +)
• N/V
• Flushed Skin
• Tachycardia
• Tachynea
• Shivering
  

Control Mechanisms for

BLOOD PRESSURE

Short-term mechanisms(2) include:

1.) Sympathetic Nervous System (SNS) releases neurotransmitters Epinephine & Norepinephrine which ↑ HR(β₁ of heart) while ↑ SVR (systemic vascular resistance; α₁ of arterioles)

2.) Vasomotor Center of the Medulla detects ↓  action potentials from baroreceptors of the carotid sinus' & aortic arch, reads that as ↓ arterial pressure, and causes ↑ in SNS activity, whose actions are listed above

Long-term mechanisms(2) include:

1.) ADH-specific mechanism whereby osmoreceptors in the hypothalamus sense ↑ plasma osmolarity and ↑ ADH secretion in response to ↑ osmolarity; this mechanism ↑ ECF which will ↑ CO & SVR

2.) RAAS (Renin-Angiotensin-Aldosterone System) mechanism whereby ↓ BP will cause the juxtaglomerular cells to release Renin into circulation which interacts with Angiotensinogen producing Angiotensin I which continues to circulate through the body. In the lungs, Angiotensin I interacts with ACE (angiotensin converting enzyme) and becomes Angiotensin II. Angiotensin II is both a powerful vasoconstrictor which ↑ SVR, and converted to Aldosterone in the Adrenal glands. Once aldosterone leaves the adrenal glands and reaches the distal tubules of the nephrons, it causes an ↑ in Na channels to ↑ sodium resorption, thereby ↑ the resorption of water and ↑ BP.

Preload is...

(& the Frank-Starling law of the heart)

 the amount of blood in the heart prior to systole; the end-diastolic volume

Frank-Starling Law of the Heart- ↑ preload increases force of contraction (i.e. ↑ SV)

Afterload is...

(give 3 examples)

impedance OR resistance  that must be overcome in order to eject blood from the LV

examples include:

1. SVR- primary determinant
2. DBP
3. Aortic Stenosis

Congestive Heart Failure is...

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

damage to the pump leads to ↓ CO

3 Locations of 

Heart Failure

(with clinical manifestations)

1. Left-Sided
2. Right-Sided
3. Biventricular 

   ---

   Left-Sided Heart Failure S/S:

Compensatory 

Mechanisms

for Heart Failure

 since ↓ CO is what the problem is, all mechanisms focus on reversing this and thereby ↑ CO

1. Brain: SNS stimulation with epi & norepi
2. Kidney: RAAS stimulation- secretion of Renin 
3. Heart: Myocardial Hypertrophy

Atherosclerosis is...

"hardening of the arteries" in which smooth muscle cells and lipids collect along the intimal surface, producing a narrowing of the luminal diameter and reduction in flow

NOTE: "ARTERIOSCLEROSIS" is a generic term meaning "hardening of the arteries"

Risk Factors of

ARTERIOSCLEROSIS

(modifiable & nonmodifiable)

Modifiable:

• smoking 
• HTN
• glucose intolerance
• hyperlipidemia
• obesity
• weight fluctuations/sedentary life-style
• ineffective stress management

Peripheral Vascular Disease is...

(5 examples include)

a general term including all diseases caused by the obstruction of large arteries in the arms & legs

examples include:

1. Arteriosclerosis/Atherosclerosis
2. Aneurysm
3. Acute Arterial Occlusion
4. Raynauds syndrome
5. Arteritis-->Thromboangitis Obliterans(aka Buerger Disease)

6 P's of 

Peripheral Vascular Disease

1. Pain
2. Pallor
3. Paresthesia
4. Polar
5. Paralysis
6. Pulselessness

3 Types of 

Angina Pectoris

(what is angina/characteristics of each)

Angina pectoris is a clinical manifestation of Coronary Artery Disease characterized by chest pain assoc. with intermittent myocardial ischemia

1. ---

   Stable (typical) Angina
2. Prinzmetal (variant) Angina
3. Unstable (crescendo) Angina

Angina 

VERSUS

Myocardial Infarction

Angina

Pain: 3-5 minutes & relieved by rest and NTG

EKG: ST elevation

Cardiac Enzymes: Not elevated

MI

Pain: 15-30 minutes, not relieved by NTG or rest; "crushing"

EKG: ST Δ's; Q waves; T wave inversion

Cardiac Enzymes: ↑ CKMB; LDH1>LDH2 (2-3days after)

Aortic Regurgitation is...

(what is it/characteristics)

when the aortic semilunar valve allows blood to leak back from the aorta into the left ventricle during diastole

• Leads to Left Ventricular Hypertrophy with eventual Left Sided Heart Failure
• S/S include ↑ SBP, ↓ DBP, Bounding Pulse
• High Pitched Blowing murmur during diastole

Mitral Stenosis is...

(what is it/characteristics)

when a stenotic mitral valve impairs blood flow from the left atrium to the left ventricle during ventricular diastole

• ---

  Leads to Left Atrial Hypertrophy
• Can lead to Chronic Pulm. HTN, Right Ventricular Hypertrophy, & Right Sided Heart Failure
• Typically sequela of rheumatic fever 10-20 years later
• Low Pitched, rumbling diastolic murmur
• S/S include: murmur, pulm. edema, dyspnea, palpitations, fatigue, hemoptysis, chest pain, recumbent cough

Normal Limits of

Cholesterol, LDLs, HDLs

Total Cholesterol <200 mg/dL

Low Density Lipoproteins <160 mg/dL

High Density Lipoproteins > 45 mg/dL for Males & > 55 mg/dL for Females

HyperTensioN

(what is it/clinical manifestations)

a consistent elevation of BP above 140 systolic and/or 90 diastolic (in adults)

Clinical Manifestations include:

• HA
• Dizziness
• N&V
• Visual Disturbances
• Renal Insufficiency

Incidence of 

HyperTensioN

& 

Risk Factors

Incidence: 

• Males
• ≥ 55 years old
• African-Americans

Rheumatic Heart Disease is...

(with clinical manifestations)

an Inflammatory disease that follows rheumatic fever, subsequent to B-Hemolytic Streptococci infection, causing valvular deformity (e.g. stenotic or regurgitative valve)

Clinical Manifestations include:

• chest discomfort
• tachycardia
• CHF
• pericardial friction rub
• murmur
• cardiomegaly
• pericardial effusion

Orthostatic Hypotension is...

(what is it/etiology)

aka Postural Hypotension

a decrease in SBP ≥ 20mmHg OR ≥ 10mmHg within 3 minutes...when moving to an upright position; an ↑ in HR by 20-30bpm may also be diagnostic

Deep Venous Thrombosis is...

(what is it/difference between deep & superficial thrombophlebitis)

acute venous obstruction due to a thrombus, trauma, thermal injury, septic state and is most commonly seen in the lower extremities; injury to the lining of the vein causes decreased circulation and stimulates the aggregation of platelets which will occlude the vessel

Deep Vein(DVT):

• extremity edema
• general leg pain
• fever
• redness
• tenderness
• positive Homan's sign
• HIGH RISK OF PE

Pulmonary Embolism

(what is it/clinical manifestations)

an undissolved detached material (blood clot, fat emboli, amniotic fluid, air, tumor, foreign bodies, parasites) that gain access to the pulmonary circulation. Once there it reaches vessels whose lumens are too small to allow its passage and it becomes stuck and occludes the lumen and obstructing perfusion

Clinical Manifestations include:

• sudden onset of pleuritic pain
• chest pain
• dyspnea
• decreased breath sounds
• coughing
• respiratory failure

Croup

(what is it/clinical manifestations/pathogenesis)

viral inflammatory disease of the larynx, trachea, & bronchi occurring in children 6 mo. - 3 y/o in the fall and early winter

clinical manifestations: BARKING cough, stridor, retractions, cyanosis

pathogenesis: the infectious agent causes inflammation along the entire airway

Asthma

(what is it/pathophys/clinical manifestations)

a lung disease characterized by airway inflammation that leads to reversible airway obstruction due to increased airway responsiveness to a variety of triggers

Pathophysiology: Hypersensitivity to triggers causes a release of leukotrienes & histamines->bronchospasm + swelling + ↑ mucus production=> airway obstruction

Clinical Manifestations include: 

• paroxysms of wheezing
• tightness in the chest
• dyspnea
• cough (both non- and production with thick mucus)

Emphysema

(what is it/pathophys./clinical manifestations)

aka COPD Type A or "Pink Puffer", a chronic obstructive respiratory condition characterized by abnormal, permanent enlargement of air spaces distal to the terminal bronchiole with destruction of their walls and without obvious fibrosis

Pathophysiology: Immune trigger (typically Smoking of >70pack/year) -> Inflammatory Response -> Neutrophils and Macrophages release proteolytic enzymes -> alveolar tissue damage

Clinical Manifestations include:

• DOE
• ↑ SOB
• Weight loss (i.e. thin)
• Labored breathing (e.g. retractions)
• Barrel chest
• Pink skin
• purse lip breathing

COPD

Type A (Emphysema)

VS.

Type B (Chronic Bronchitis)

Type A  | VS |  Type B

"pink puffer" | "blue bloater"

Thin | Obese

        Mild Hypoxemia | Hypoxemia & Hypercapnia

  Few secretions | Copious secretion

      | ↑ Hct

                          | Cor Pulmonale       

Types of

Fractures (Fxr)

(8)

• Transverse
• Spiral**
• Longitudinal
• Oblique
• Comminuted
• Impacted
• Greenstick
• Stress

Complications

of Fractures

• Delayed wound healing (3 mos. - 1 year) 
• Fat Embolism Syndrome: Fat globules released from yellow marrow into circulation -> gets stuck in pulmonary circulation (PE) -> Lipase released to degrade embolus -> Fatty acid irritation of capillary & alveolar walls
  • S/S: LOC Δ's, restless, agitated, confusion, dyspnea, ↑ RR, ↑ HR, ↑ Temp, Petechiae
• Compartment Syndrome: swelling within an unyielding structure or compartment of a nonelastic tissue or device (e.g. cast)
  • Forearm & Leg most common sites
  • S/S: pain distal to injury, ↓ CRT, mottled or cyanotic skin
  • 4-6 hrs after onset=> irreversible damage
  • Late Signs include the 6 P's: Pallor, Pain, Paresthesia, Polar, Paralysis, Pulseless

OsteoArthritis

(aka/what is it/clinical manifestations)

aka "Wear & Tear" disease

a common Degenerative Joint Disease  characterized by progressive loss of articular cartilage and by formation of new bone from subchondral bone at joint margins

Clinical Manifestations include:

• enlarged osteoarthritic joint only
• crepitus with movement
• pain
• Heberden's nodules(distal to joint) & Bouchard's nodules (proximal to joint)

Rheumatoid Arthritis

(what is it/pathophys./clinical manifestations)

a systemic, inflammatory, connective tissue disease of unknown cause; joint involvement is symmetric; other systems affected include integumentary, ocular, otolaryngologic, pulmonary, cardiac, GI, renal, neurologic, & hematologic.

Pathogenesis: UNKNOWN Ag activates immune system in synovial tissue of joints -> Both B & T Lymphocytes along with Macrophages enter tissue -> B Cells produce IgG Ab that treat IgG as foreign and not self -> Complement activated -> enhanced immune response & recruits more immune cells -> hydrolytic enzymes and inflammation perpetuating mediators released into synovium -> hypertrophying synovium & perpetual inflammation

Clinical Manifestations include:

• morning stiffness
• soft tissue swelling of 3+ joint areas
• swelling of one wrist, MCP, PIP
• subcutaneous nodules

a nonspecific defense mechanism characterized by TUMOR, DOLOR, RUBOR, CALOR & loss of function. 

Purpose: 

1. to neutralize and destroy invading agents
2. limit the spread of harmful agents
3. prepare damaged tissue for healing

Vasoactive Chemicals released during the Inflammatory Process include...

• Histamine
• Prostaglandins
• Leukotrienes

  ---

  Histamine is an early mediator of the inflammatory response; potent vasodilator;bronchial constriction; ↑ mucus production

  ---

  Prostaglandins contribute to vasodilation & increased permeability; aids in neutrophil chemotaxis; enhances sensitivity of pain receptors

Autoimmune Disease

what is it?

an individual's immune system recognizes its own cells as foreign and mounts an immune response that injures self tissues

HIV/AIDS

Etiology & Transmission

Human Immunodeficiency Virus/Acquired Immune Deficiency Syndrome

AIDS is defined as the last stage of infection with HIV

Etiology of HIV--> retrovirus' HIV-1 & HIV-2 found in USA, Europe, Australia, & Central Africa, and West Africa, India  respectively. HIV gains access to CD4 cells by attaching to the CD4 receptor on the cell surface.

Transmission--> sexual via semen or vaginal/cervical secretions; parenteral via blood or blood products; perinatal via placental transfer, during delivery, or in breast milk.

*Transmission via urine, saliva, tears, cerebrospinal fluid, and feces NOT KNOWN.

Cardinal Signs 

of

Inflammation

(5)

• Rubor = redness

  ---

• Tumor = swelling

  ---

• Dolor = pain

  ---

• Calor = heat

  ---

• Loss of function

SIADH

pathophys./clinical manifestations

 Pathophys.- excessive secretion of ADH which leads to excessive water retention which leads to dilute plasma, hyponatremia, and water intoxification

Clinical Manifestations- 

• hyponatremia
• lethargy
• confusion
• cerebral edema
• seizures
• coma
• muscle cramps
• weakness
• ↓ UOP
• fluid retention
• wt. gain

Grave's Disease

(hyperthyroidism)

pathophys./clinical manifestations

 Pathophys.- IgG autoantibodies bind to and stimulate TSH receptors on thyroid which ↑ thyroid hormone( T4/thyroxine & T3/triiodothyronine) and leads to hypermetabolic state

Clinical Manifestations:

• thyroid hyperplasia (Goiter)
• Exophthalmos
• warm, moist skin
• thin, fine hair
• ↑HR & BP
• hyperreflexia
• fine tremor
• "lid lag"

Myxedema

(description/clinical manifestations)

Diabetes Insipidus

(aka/pathophys./clinical manifestations)

AKA Polyuria

Clinical Manifestations:

• ↓urine specific gravity
  
• polydipsia
• hypernatremia
• nocturia in adults/enuresis in children
• dehydration
• neurological symptoms

ISCHEMIA

what is it/consequences

the interruption of blood flow to an area

Consequences:

• ↓ O2 supplies--> anaerobic metabolism of glucose--> ↑ lactic acid --> ↓ pH --> ↓ protein and enzyme function
  
• Accumulation of metabolic wastes
• ATP-Dependent pumps (Na+/K+) fail as ATP  stores ↓--> Na rushes in and H20 follows causing swelling

  ---

  MOST damage occurs after the blood supply to the tissues has been restored- a so called reperfusion injury

Acute Lymphoblastic Leukemia

(what is it/clinical manifestations)

a malignant disorder of the lymphoid cell lineage; lymphoblasts (immature B & T lymphocytes)  accumulate in large numbers in the blood and bone marrow which crowds out the production of normal RBC's, platelets, and leukocytes; circulating lymphoblasts are poorly functioning cells and do not provide effective immunocompetence

Clinical Manifestations include:

• abrupt onset of symptoms
• bone pain
• bruising
• fever
• infection
• anorexia
• fatigue
• abd. pain
• possible enlargement of spleen, liver, & lymph nodes