patho exam 2 combined

renal and urinary systems functions

• maintaining fluid electrolyte balance

• maintain acid-base balance

  • excrete hydrogen

• regulate BP

• release erythropoietin to stimulate RBC production

  • when there isn’t enough oxygen in the blood, bone marrow cells get signaled to make RBC

• activation of vitamin D

the nephron

• functional unit of kidney

• glomerulus: bundle of capillaries that sit within Bowman’s capsule

  • site of filtration → filters out sodium (water follows), potassium, hydrogen, phosphate

• urine flows from Bowman’s capsule → proximal convoluted tubule → loop of Henle → distal convoluted tubule → collecting duct

• blood vessels that surround the nephron are involved in reabsorption of solutes and water

  • at the end, you will have some sort of concentrated urine depending on what your body needs

    • could be concentrated or diluted depending on what your body reabsorbs

regulation of urine output, fluid balance and BP

• several factors involved

  • juxtaglomerular cells (like stretch receptors that gauge what the blood pressure is)

    • release renin in response to low BP

    • renin activates RAAS to increase BP (retain fluid and water)

  • antidiuretic hormone (ADH)

    • released by posterior pituitary in response to decreased BP or increased serum osmolality

    • ADH promotes fluid reabsorption from collecting duct

      • just tells collecting ducts to reabsorb water (not sodium, just water)

  • ANP and BNP

    • released by heart in response to stretching

    • promotes excretion of Na and H2O

      • decreases fluid overload

      • when there is too much fluid in your blood, it will overload the ventricles and atria and cause them to stretch

renin-angiotensin-aldosterone system

• renin is released from juxtaglomerular cells in response to low BP or sympathetic stimulation

• renin converts angiotensinogen (produced by liver) into angiotensin I

• angiotensin converting enzyme (ACE - produced by lungs) converts angiotensin I into angiotensin II

• angiotensin II has 2 main functions

  • vasoconstriction

  • stimulates release of aldosterone from adrenal cortex

regulation of acid base balance

• during acidotic states, kidney promotes:

  • excretion of H+

  • reabsorption of HCO3

  • synthesizes of new HCO3

• during alkalotic states, kidney promotes:

  • retention of H+

simple cysts

• common

  • single or multiple

  • unilateral or bilateral

  • usually very small

    • < 1 cm

  • usually don’t produce signs or symptoms

    • may cause flank pain

    • may cause hematuria

    • may become infected

autosomal dominant polycystic kidney disease (ADPKD)

• most common renal cystic disease

• etiology

  • two gene mutations that lead to excessive growth and differentiation of epithelial cells

  • result is destructive, fluid-filled cysts in the kidney and other organs

  • can lead to fibrosis

• cysts may detach and continue to grow

• damage to renal tissue believed to be due to

  • inflammatory mediators

  • apoptosis of renal tubule cells

autosomal dominant polycystic kidney disease: clinical manifestations

• may be asymptomatic for decades

• flank pain

• cysts can bleed or become infected

• can also lead to issues elsewhere

  • cysts in liver and pancreas

  • diverticuli

  • aneurysms in cerebral arteries

  • heart valve issues

renal calculi (nephrolithiasis)

• “kidney stones” → masses of crystals, proteins or other substances that obstruct the flow of urine

• most develop in kidney, but may start anywhere in urinary tract

• composed of particles normally excreted in urine

• many factors involved in development

  • high concentration of these particles in bloodstream

    • start precipitating out and coalescing into stones

  • hydration status

    • like it’ll be a normal amount of solution, but there’s not enough water for it to dissolve so it’ll form stones instead

  • anatomy of urinary tract

  • diet and intestinal absorption

  • metabolism

  • UTIs

renal calculi: risk factors

• requires supersaturated urine

• depends on pH of urine and concentration of ions

  • alkaline urine usually more likely to develop renal calculi

• also requires a nucleus that facilitates stone formation

  • small cluster of crystals held together by ionic force

  • organic materials produced by epithelium

renal calculi: calcium stones

• most common (70-80%)

• conditions that increase serum Ca or decrease fluid volume will increase risk of calcium stones

  • hyperparathyroidism (parathyroid is for the regulation of calcium)

    • the parathyroid is taking too much calcium from the bones and putting it in the blood

    • can lead to multiple myeloma

  • increased reabsorption of bone

renal calculi: struvite stones

• magnesium ammonium phosphate (struvite) stones

  • often associated with bacterial infection / UTI

  • more common in people AFAB

  • bacteria secrete urease

    • urease converts urea → ammonia

    • ammonia makes urine alkaline

    • alkaline urine promotes formation of stone

  • can grow into staghorn calculi

renal calculi: uric acid stones

• more common in individuals who excrete large amounts of uric acid in their blood (those with gout or abnormal metabolism of purines)

• also associated with high amount of purines in diet (meat, beer)

• not visible on x-ray

renal calculi: cysteine stones

• more common in children

• an amino acid that precipitates more readily in acidic urine

• conditions that increase cysteine in blood (genetic predisposition) will increase cysteine in urine and increased risk of cysteine stones

renal calculi: clinical manifestations

• flank pain radiating to the groin

• may be accompanied by nausea and vomiting

renal calculi: summarized

• calcium

  • most common (70-805)

  • any condition that increases calcium concentration in blood (hyperparathyroidism, conditions that remove Ca from bone, etc.)

  • also common with low urine volume (precipitation)

• magnesium ammonium phosphate (struvite)

  • can only form in alkaline urine

  • requires bacterial infection

  • can result in staghorn calculus (requires lithotripsy)

• uric acid

  • caused by conditions that produce high uric acid in blood (gout)

  • not visible on x-ray

• cysteine

  • more common in children

  • genetic problem with renal transport of cysteine

  • similar to struvite, but no UTI

urinary tract infections (UTi)

• inflammation of urinary epithelium (can occur anywhere)

• most often caused by bacterial infection

  • most are GI bacteria that enter through urethra due to poor hygiene

  • some can enter from bloodstream (more common among the immunocompromised)

• most common pathogen is Escherichia coli

  • klebsiella, proteus, Enterobacter, pseudomonas also can cause UTI

• urine from bladder normally washes out bacteria in urethra

  • increased risk when this is disrupted

• uncomplicated → bladder infection in someone with no other comorbidities

• complicated → when the infection goes up and infects the kidneys or when the person is pregnant or if they have comorbidities

urinary tract infection: normal host defenses

• washout phenomenon

  • washes pathogens out of urethra with urination

• protective mucin layer

  • lines bladder - prevents attachment and infection

• ureteral peristalsis

  • moves urine and pathogens down from kidneys

• low pH of urine inhibits bacterial growth

  • like if you drink cranberry or graprefruit juice

• normal flora of periurethral area

  • lactobacillus → defends against uropathogens

urinary tract infection: contributing factors

• virulence of pathogens

  • presence of pili or fimbriae that help pathogens adhere

    • fimbriae → finger like projections that come out of the pathogen that help create anchor points (so they aren’t able to get washed out when the person urinates)

• decreased urinary flow, ureteral obstruction or reflux

• catheterization

  • allows the bacteria to climb up

• pregnancy

  • baby presses on ureter and has the potential to push the urine backwards

• use of antibiotics that kill normal flora

• diabetes mellitus

  • aren’t able to metabolize glucose → all the excess glucose in the urine serves as food for the bacteria

acute cystitis

• inflammation of bladder

• most common site of UTI

• patho

  • often due to retrograde movement of bacteria up urethra

  • e. coli is most common

  • some strains possess fimbriae that that help them attach to epithelium and flagella that help them move up urinary tract

  • many strains of e. coli release toxins that induce inflammation

acute cystitis: clinical manifestations

• inflammation → edema in bladder → stimulates stretch receptors that create a sensation of fullness

  • frequency

  • urgency

  • dysuria (pain when urination)

• suprapubic / low back pain

• hematuria (hemorrhagic cystitis → bladder becomes so inflamed that it starts to bleed)

  • blood in urine

• cloudy / foul smelling urine

• older adults often present with mental status change

acute pyelonephritis

• infection of upper urinary tracts (kidneys and ureters) - more common in people AFAB

• patho

  • usually the result of ascending infection from bladder

    • also can gain access from bloodstream (less common)

  • inflammation usually affects renal tubules in the renal pelvis, calyces and medulla

  • BUN (blood urea nitrogen) and creatinine tests for kidney function

    • also glomerular filtration rate (GFR)

acute pyelonephritis: clinical manifestations

• fever

• malaise

• chills

• flank pain

• symptoms of UTI

  • urgency, frequency, etc. due to stretching of bladder

glomerular disease

• glomerulus is a net of capillaries within Bowman’s capsule

• filtration takes place

• glomerulonephritis → inflammation of glomerular structures

  • 2nd leading cause of kidney failure in US

• broken down into 2 broad categories based on the symptoms that the person experiences

  • nephritic and nephrotic

glomerular disease: causes

• immunologic → most common

  • antibodies reacting with glomerular antigens (type II HSR)

    • IgG or IgM binds to a receptor on a cell and leads to inflammation

  • antigen-antibody complexes trapped in glomerulus (type III HSR)

    • antibody creates a complex around a cell (bind to a structure in circulation) then binds to a nephron or blood vessel and causes inflammation there

• non-immunologic

  • diabetic nephropathy

    • create molecules that harm the nephron

  • hypertensive nephropathy

  • toxic medications, etc.

• hereditary

glomerular disease: pathologic changes

• three main changes associated with glomerular disease

  • proliferation: increase in cell number and formation of “crescents”

  • thickening of basement membrane

  • sclerosis/fibrosis: accumulation of proteins and collagen that obstruct glomerulus

• two broad categories of primary glomerular diseases based on presentation

  • nephritic syndrome

  • nephrotic syndrome

nephritic syndrome

• glomerular diseases characterized by INFLAMMATION of glomeruli

• clinical presentation

  • oliguria

    • because of the inflammation, you aren’t going to be able to filter things out (less urine)

  • hypertension

    • since you can’t excrete the water, BP increases = hypertension

  • azotemia (nitrogenous wastes in blood)→ proteinuria not as pronounced as in nephrotic syndrome

    • you can’t excrete BUN and creatinine

  • hematuria → blood in urine

• specific conditions

  • post infectious glomerulonephritis

  • rapidly progressive (crescentic) glomerulonephritis

• ITIS = ITIC

nephrotic syndrome

• glomerular diseases characterized by increased glomerular PERMEABILITY

• clinical presentation

  • profound proteinuria

    • large molecules are going to get dumped into urine (albumin is most common protein in blood)

  • hypoalbuminemia → edema

    • since all the albumin is in the urine, there won’t be a lot in the blood vessels (albumin attracts water into vessel)

    • water then stays in the tissue and leads to edema

  • lipiduria with compensatory hyperlipidemia

    • lipids in urine because of permeability

    • however the liver overcompensates for the loss of lipids in urine so there will be an increase of lipids in blood

• specific conditions

  • minimal change disease

  • membranous nephropathy

  • focal segmental glomerulosclerosis

    • collagen in glomerulus and hardens it

• O in OTIC = HOLE

nephritic syndrome key points

• major abnormality → inflammation

• characteristics

  • decreased glomerular filtration → oliguria

  • increased nitrogenous wastes → azotemia

  • poor kidney function leads to HTN

  • damaged capillaries allow RBCs to escape → hematuria

  • some proteinuria, but not significant

nephrotic syndrome key points

• main abnormality → increased glomerular permeability

• characteristics

  • massive proteinuria

  • hypoalbuminemia → edema

  • lipiduria → overcompensation of LDL by liver

post-infectious glomerulonephritis

• most common in children

• nephritic syndrome (ITIS = ITIC)

• post infectious = after an infection

  • Like if you had strep throat, then you have kidney malfunction, you probably have this (it usually follows strep throat)

• patho

  • most often follows a group A beta hemolytic streptococcal infection

  • antibodies produced against group A beta hemolytic streptococcal antigen

  • antibodies bind to antigens in circulation and form immune complexes

  • immune complexes aggregate in glomerulus and promote inflammation (type III hypersensitivity)

  • proliferation of glomerular cells and infiltration by leukocytes follows

post infectious glomerulonephritis: clinical manifestations

• nephritic syndrome 1-2 weeks after strep throat infection

  • oliguria

  • hypertension

  • azotemia

  • hematuria

• fever

• malaise

rapidly progressive (crescentic) glomerulonephritis

• glomerular disease characterized by development of cellular crescents in the glomerulus and rapid loss of renal function

• nephritic

• patho

  • initiated by either

    • immune complexes that deposit in glomerulus and promote inflammation (type III hypersensitivity)

    • antibodies (IgG) against glomerular basement membrane that stimulate inflammation (type II hypersensitivity)

  • inflammation promotes proliferation of Bowman capsule epithelial cells and infiltration by leukocytes to create crescent that obliterates Bowman’s space

  • sometimes IgG cross reacts with alveolar basement membrane to produce pulmonary hemorrhage in addition to renal failure (Goodpasture syndrome)

    • if it affects kidney and lung = goodpasture

rapidly progressive (crescentic) glomerulonephritis: clinical manifestations

• nephritic syndrome

  • hypertension

  • azotemia

  • hematuria

  • oliguria

nephritic syndrome summary

• examples

  • post infectious glomerulonephritis

    • follows group A beta-hemolytic strep throat

    • immune complexes in glomerulus stimulate inflammation

  • rapidly progressive glomerulonephritis

    • rapid proliferation of glomerular cells

    • recruitment of monocytes and macrophages that obliterate Bowman’s space

    • creates a “crescent” shaped blockage

• manifestations

  • decreased glomerular filtration → oliguria

  • increased nitrogenous wastes → azotemia

  • poor kidney function leads to HTN

  • damaged capillaries allow RBCs to escape → hematuria

  • some proteinuria, but not significant

minimal change disease (lipid nephrosis)

• most frequent cause of nephrotic syndrome in children

• relatively benign

• patho

  • believed to be due to immune reaction that results in epithelial cell damage

  • result is increased permeability and proteinuria

  • often associated with respiratory illness

minimal change disease (lipoid nephrosis): clinical manifestations

• nephrotic syndrome

  • profound proteinuria / hypoalbuminemia

  • edema

  • lipiduria with compensatory increase in lipids in the blood

• renal function remains good, however

membranous nephropathy

• glomerular disease associated with thickening of glomerular basement membrane

• one of the most common causes of glomerular disease

• comparable to a type III HSR

• patho

  • deposits of antigens and IgG antibodies form between basement membrane of glomerular capillaries and Bowman’s capsule

  • activation of inflammation

  • increased capillary permeability

  • thickening of basement membrane

membranous nephropathy: clinical manifestations

• nephrotic syndrome

  • proteinuria

  • edema

  • lipiduria

focal segmental glomerulosclerosis

• glomerular disease characterized by sclerosis of some glomeruli (not all)

• more common in persons of African-American and Hispanic heritage

• patho

  • believed that a circulating cytokine induces epithelial cell injury

  • plasma proteins and extracellular matric proteins (collagen) become deposited

  • scar tissue forms → sclerosis

focal segmental glomerulosclerosis: clinical manifestations

• nephrotic syndrome

• proteinuria

• edema

• lipiduria

nephrotic syndrome: key points

• examples

  • minimal change disease

    • most common in children

    • may be related to infection

    • no HTN and rare loss of kidney function

    • responds well to corticosteroids

  • membranous nephropathy

    • most common in adults

    • immune complexes deposit on glomerular basement membrane

    • basement membrane thickens

    • stimulates release of enzymes that destroy capillary walls

  • focal segmental glomerulosclerosis

    • deposit of collagen in glomeruli

    • damages glomerular tissue

    • more common in people of Hispanic and African-American / Caribbean-American heritage

• manifestations

  • massive proteinuria

  • hypoalbuminemia → edema

  • lipiduria → overcompensation of LDL by liver

glomerular disease diagram

Wilms tumor

• one of the most common primary neoplasms of children

• tumor composed of elements resembling fetal tissue

• due to genetic mutation

• associated with several congenital abnormalities

  • aniridia

    • they don’t have an iris (colored portion of eye)

  • hemihypertrophy

    • one half of the body is bigger than the other side (like one arm is bigger than the other)

• clinical manifestations

  • large, asymptomatic abdominal mass

  • HTN

    • releases epinephrine which activates the fight or flight response and increases HTN

• managed with surgery and chemotherapy

• good prognosis - 5 year survival 90%

renal cell carcinoma

• cancer kidneys

• accounts for 80% of renal neoplasms

• risk factors

  • smoking

  • obesity

  • hypertension

  • NSAIDs

  • exposure to industrial solvents, asbestos, heavy metals

renal cell carcinoma: clinical manifestations

• hematuria

• dull flank pain

• palpable flank mass in think patients

• weight loss, fatigue, fever, anemia if cancer is advanced

acute kidney injury (AKI)

• sudden decline in renal function

• affects 5% of hospitalized patients

• mortality of 50-50%

• decreased in glomerular filtration with decreased urine output and increased retention of nitrogenous wastes, K and PO4

• three possible etiologies

  • pre-renal: a disorder characterized by decreased renal perfusion

  • intra-renal: a disorder characterized by poorly functioning renal tissue

  • post-renal: a disorder characterized by obstruction of the urinary tract

pre-renal etiology

• most common cause of AKI

• problem getting blood to kidney

• patho

  • decreased renal perfusion results in decreased filtration

  • reduced filtration promotes retention of fluids and nitrogenous wastes

  • may be due to

    • hypovolemia

    • sepsis

    • decreased cardiac output (MI or HF)

    • renal artery constriction / stenosis

      • artery is stiff

intra-renal etiology

• kidney can’t make urine

• patho

  • often the result of acute tubular necrosis (ATN)

  • also can be the result of glomerulonephritis, vascular disease (HTN, DIC), or disease of the interstitial tissue (cancer, infection)

• two categories of ATN

  • ischemic ATN

    • damage to renal cells is due to prolonged ischemia and hypoxia

  • nephrotoxic ATN

    • damage of renal cells is due to a toxic (IV contrast, antibiotics (aminoglycosides → nephrotoxic), heavy metals (mercury, arsenic), bacterial toxins)

acute tubular necrosis (ATN)

• destruction of renal tubule epithelial cells with suppression of renal function

  • damage leads to necrosis of epithelial cells

  • epithelial cells obstruct lumen of renal tubule

  • increased pressure in lumen causes decreased glomerular filtration

  • fluid leaks from nephron into interstitial tissue

• usually reversible → depends on:

  • recovery of injured cells

  • clearance of necrotic cells

post-renal etiology

• uncommon

• can’t get urine out of the body

• patho

  • obstruction of urinary tract bilaterally

  • obstruction causes increase pressure in lumen of urinary tract (ureters, etc)

  • GRF gradually declines

  • several hours of anuria and flank pain → polyuria

acute kidney injury (AKI): clinical manifestations

• progressive

1. onset/initiating phase

• time from precipitating event to injury

2. oliguric phase

• sudden, significant decline in GFR

• retention of nitrogenous wastes (BUN, creatinine, etc)

• low urine output

• fluid retention (edema, pulmonary congestion, HTN)

• neurologic symptoms may develop due to buildup of nitrogenous wastes)

3. diuretic phase

• kidneys heal

• urine output improves → diuresis

• nitrogenous wastes don’t improve yet

4. recovery phase

• filtration returns to normal

• nitrogenous wastes improve

• tubular edema resolves

• Oo, Dr

  • onset / initiating

  • oliguric

  • diuretic

  • recovery

chronic kidney disease (CKD)

• progressive loss of kidney function due to permanent loss of nephrons

• often due to systemic disease (HTN, DM, SLE)

• progressive loss of renal function

• symptoms won’t appear until renal function is below 25% normal

• patho

  • nephron loss begins in response to secrete or prolonged injury

  • persistent injury → fibroblast proliferation → focal segmental glomerulosclerosis and interstitial fibrosis

chronic kidney disease: clinical manifesations

• azotemia (retention of urea, creatinine, and other nitrogenous wastes)

  • creatinine is released by muscle and is excreted by kidney

  • can lead to uremic syndrome (nausea, vomiting, diarrhea/constipation, pruritis → itching)

    • how the body reacts to elevated levels of nitrogenous wastes

• metabolic acidosis

  • H+ is not excreted

  • may require dialysis

• fluid and electrolyte imbalances

  • potassium

    • K+ cannot be excreted - levels can rise and become life threatening

      • helps with function of heart → too high/too low can develop arrhythmias

    • normal levels of potassium = 3.5 - 5

    • normal albumin also 3.5 - 5

  • Na+ and H2O

    • Na and H2O retention can occur → HTN

  • Ca and PO4

    • abnormalities will be noticed late

    • kidneys cannot excrete PO4 → serum PO4 will be increased

    • PO4 binds to Ca in circulation → hypocalcemia

      • If you have a lot of phosphate in blood, then it will bind with calcium and make the levels of the blood go down (bc they’re binding together to make phosphate-calcium)

      • normal calcium levels is 9 - 11

    • hypocalcemia may stimulate release of PTH from parathyroid glands → increased bone reabsorption

      • Parathyroid gland will see that calcium levels are down and then will pull calcium out of the bone → osteoporosis and risk for fractures

    • kidneys cannot activate vitamin D → gut cannot absorb Ca well

• proteinuria

  • due to renal damage

• anemia (HGB < 12 for people AFAB / < 13.5 for people AMAB)

  • kidney cannot sense low oxygen tension or secrete erythropoietin

  • Kidney secretes erythropoietin to signal the bone marrow to make more RBC (But if kidneys fail, they can’t send out that signal = anemia)

• neurologic complications

  • due to uremia and hyperkalemia

  • nitrogenous wastes and K+ damage neurons

  • increased K+ associated with increased neuromuscular excitability

    • hiccups

    • muscle cramps

    • muscle twitching

  • change in mental status (impaired memory, concentration and judgement, confusion, etc.)

bladder cancer

• most frequent form of urinary tract cancer in the US

• cause is unknown

  • may be linked to carcinogens excreted into urine and stored in bladder

    • occupational exposure to dyes, rubber, textiles, paint, petroleum

    • cigarette smoking accounts for 30-50%

• clinical manifestations

  • painless hematuria

  • frequency, urgency, dysuria

• managed with surgery - chemotherapy may be attempted for advanced cancer

alveolar anatomy

• location of gas exchange - large surface area

• several cell types are present in alveolus

  • Type I pneumocyte

  • type II pneumocyte

  • alveolar macrophage

type I pneumocyte

• make up 95% of alveolar epithelium

• provide structure

• easily damage

• where gas exchange occurs

type II pneumocyte

• secrete surfactant - prevents alveolar collapse (atelectasis)

• repair the epithelium by producing type I pneumocytes

• what helps the alveoli from not sticking together

alveolar macrophage

• phagocytic cells responsible for innate immunity

  • protect against infections

measures of oxygenation: PaO₂

• partial pressure of oxygen in arterial blood (normal > 80 mmHg)

  • a measure of how much pressure your oxygen exerts within your blood vessels

  • evaluated on the ABG

  • as PaO₂ increases, more O2 is forced into HGB

  • O2 continues to bind to HGB until the HGB is saturated

measures of oxygenation: SaO₂

• oxygen saturation

• describes the % of HGB that is bound to O2

  • measured by pulse ox

ventilation / perfusion (V/Q)

• diffusion of O2 from alveolus into blood also is dependent on:

  • ventilation (V): the amount of air getting to the alveoli

  • perfusion (Q): the amount of blood making it to the alveoli

• a V/Q mismatch is the most common cause of hypoxemia

pulmonary function tests (FEV1)

• forced expiratory volume in one second

  • measure amount of air expelled in one second following full inspiration

• the person takes a big deep breath in and then blows out forcefully

  • measurement to figure out how much is blown out in one second

    • should be pretty high

pulmonary function tests (FVC)

• forced vital capacity

  • the total amount of air that can be expired following full inspiration (not limited to 1 second)

• person takes a big deep breath in and then blows out

  • see how much air they can empty from their lungs after a full inspiration

  • seeing how much total air volume exists in the lungs

FEV1 / FVC ratio

• < 0.7 is indicative of obstructive lung disease

the common cold

• most common respiratory tract infection

• etiology: viruses

  • rhinoviruses are most common

  • parainfluenza virus

  • respiratory syncytial virus (RSV)

  • coronaviruses

  • time of year determines specific virus

  • most often spready by direct contact

    • less common by aerosol

common cold: clinical manifestations

• begins with feeling of dryness/stuffiness in nasopharynx

• clear, watery nasal secretions follow

• tears

• swollen mucous membranes

• post-nasal drip → sore throat

• 2 day incubation period where you don’t see many symptoms

• virus promotes inflammation

  • increased vascular permeability → that’s what leads to nasal secretions

  • vascular dilation

• management

  • self limiting

  • rest and treat symptoms

  • vitamin c

  • chicken soup

rhinosinusitis

• inflammation of nasal sinuses

• patho

  • upper respiratory infection (usually viral) promotes mucosal swelling

    • swelling blocks flow out of sinuses

    • fluid, mucous, pressure increase

  • nasal polyps also can impede flow

  • can be acute or chronic

    • chronic lasts > 12 weeks

    • usually due to bacterial or fungal infection

rhinosinusitis: clinical manifestations

• facial pain

  • the pt will have pressure wherever their paranasal sinuses are

  • if you were to palpate those areas, it would feel warm and it would hurt

• headache

• purulent nasal discharge

  • if it was a bacterial infection

• fever

epiglottitis

• dramatic, potentially fatal inflammation of the epiglottis and pharynx

• etiology

  • often due to bacterial infection (S. pyogenes, S. pneumonia and S. aureus are most common)

epiglottitis: clinical manifestations

• pale

• lethargic

• sitting with mouth open and chin thrust forward

• muffled voice

• stridor

• drooling → they can’t swallow the saliva they are producing

• anxiety

• inspiratory retractions (muscles)

• flaring of nares

epiglottitis: nursing considerations

• DO NOT examine throat or attempt culture

• complete obstruction of airway could be imminent → death

• medical emergency - establish airway immediately

influenza

• viral respiratory infection

• three types: A, B and C

• influenza A and B cause seasonal flu epidemics

• subtypes of influenza A are categorized by proteins on the surface

  • hemagglutinin (H): helps virus attach to respiratory epithelium

  • neuraminidase (N): helps newly formed virus release from epithelium

  • many possible combos: H1N1, H5N1, etc.

influenza: virulence

• more contagious than bacterial infection

• spready by inhaling infected droplets or touching infected surfaces

• incubation 1-4 days

• infectious 1 day before symptom onset

• airborne transmission

influenza: patho

• virus infects upper airway

  • virus attaches to respiratory epithelial cells (hemagglutinin)

  • virus enters respiratory epithelial cells to replicate

  • epithelial cells are damaged during viral replication

    • fluids and inflammatory mediators leak out of epithelial cells

    • inflammatory mediators promote inflammation (redness and swelling of respiratory tract)

    • damage to goblet cells = reduced mucous secretion

    • damage to ciliated columnar cells → reduced ciliary motion

  • underlying basal cells are exposed

    • the only thing that will be left are the basal cells and basement membrane

    • holes between them allow extracellular fluid to escape (runny nose)

influenza: virus spread to lower airway

• bronchial and alveolar epithelial cells are shed

• single layer of basal cells is left

• increased likelihood of bacterial attachment and infection

• pneumonia can develop from viral or bacterial infection

  • as air moves lower into your airway, it will start killing more cells which can lead to pneumonia (viral pneumonia)

  • since many of the cells of the epithelium are stripped away, bacteria can come down and attach to the free spots (bacterial pneumonia)

influenza: clinical manifestation

• abrupt onset of fever and chills

• rapid onset of malaise (characteristic of flu)

• muscle aches

• headaches

• nasal discharge

• non-productive cough

• sore throat

• viral pneumonia may occur → rapid progression of symptoms

• secondary complications → bacterial pneumonia, croup (in children)

influenza prevention

• annual vaccine to reduce risk in all people over 6 years of age

  • if a vaccine is good against 3 strains = trivalent

    • 4 strains = quadvalent

• particularly important in

  • clients with chronic respiratory illness (emphysema, asthma, etc)

  • clients who are immunosuppressed

  • older adults

  • young children

pneumonia

• inflammation of lower respiratory tract

• commonly caused by infectious agents

• can be caused by non infectious agents (inhaled toxins, hot air, etc.)

• 8th leading cause of death in the US

risk factors for pneumonia

• older age

• immunosuppression

• chronic respiratory disease (COPD)

• smoking

• altered level of consciousness

  • usually when you aspirate something, you are able to cough it up

  • but with ALC, you lose that ability

• endotracheal tubes

pneumonia: classifications

• setting: community acquired vs hospital acquired

• type of agent: typical (bacterial) vs atypical (viral or mycoplasma pneumonia)

• pattern of distribution: lobar (consolidation of one lobe) vs bronchopneumonia (patchy)

pneumonia: community acquired (CAP)

• occurs outside hospital or within 48 hours of admission

  • streptococcus pneumoniae is most common

  • haemophilus influenza

  • legionella pneumophila

  • influenza

• easier to treat compared to HAP

pneumonia: hospital acquried (HAP)

• occurs 48 hours after admission or more

  • many have antibiotic resistance

  • pseudomonas aeruginosa

    • very distinct smell when it’s in the mucus

  • klebsiella pneumonia

acute bacterial pneumonia

• aspiration of secretions from oropharynx is most common

  • streptococcus pnumoniae is the most common organism

  • some bacteria gain access through inhalation (Legionella)

  • endotracheal tubes bypass upper airway defenses (cough, mucociliary blanket, etc.) and increase risk

  • normally microorganisms are destroyed by alveolar macrophages or can be coughed out

  • loss of cough reflex, reduced function of cilia, damage to endothelium and suppression of the immune system increase risk of colonization

pneumococcal pneumonia

• model bacterial pneumonia

• aspiration of streptococcus pneumoniae into lower airway

• alveolar macrophages ingest S. pneumoniae

• macrophages release inflammatory mediators → inflammation

steps in pneumococcal pneumonia

• stage 1: congestion

  • alveoli and surrounding tissue fill with protein rich fluid (edema) → because of increased capillary permeability from inflammation

    • destroys the type II pneumocytes (the ones that keep the alveoli open and provide surfactant)

  • bacteria not ingested by macrophages multiply in edema and spread to adjacent alveoli

• stage 2: red hepatization

  • RBCs, neutrophils and fibrin accumulate in the alveoli and interstitial tissue → consolidation

    • neutrophils will show up (the first responders) → recruit fibroblasts that produce collagen

    • more red cells will show up because of the vasodilation

• stage 3: grey hepatization

  • RBCs dissipate and leave neutrophils and fibroblasts

    • collagen from the fibroblasts aren’t an elastic molecule which will make your lungs stiff

  • neutrophils and macrophages continue to fight the infection

• stage 4: resolution

  • enzymes or macrophages remove fluid and debris

bacterial pneumonia

• clinical manifestations

  • cough, dyspnea, fever

  • crackles

  • signs of consolidation (tactile fremitus, egophony, whispered pectoriloquy)

• prevention

  • prevent aspiration

  • remove ETTs when possible

  • vaccination

viral pneumonia

• influenza is the most common cause

• usually milder, self-limiting but can set the stage for bacterial infection

  • doesn’t create the same consolidation (not as noticeable on x-ray)

• viral infections damage ciliated epithelial cells and goblet cells

  • virus attaches to respiratory epithelial cells

  • virus enters respiratory epithelial cells to replicate

  • epithelial cells are damaged during viral replication

  • underlying basal cells are exposed

  • bronchial walls become edematous and infiltrated by leukocytes → pneumonia

    • no fluid accumulation / consolidation → not visible on x-ray

tuberculosis

• infection caused by Mycobacterium tuberculosis

  • possesses waxy capsule

  • protects itself from immune system

• affects lungs mainly but can affect other organs

• risk factors

  • crowded living environments (barracks, dorms, prisons, nursing homes, etc.)

  • people without a fixed residence

  • people with substance use disorders

  • lack of screening

tuberculosis: spread

• spread by respiratory droplets (coughing, sneezing, etc.)

  • droplet evaporates

  • bacteria remains suspended in air and inhaled

  • very contagious

tuberculosis: strong immunity

• approx. 10% of those exposed will develop disease

• in someone with an intact immune system, the bacteria is usually contained in a granuloma

  • 95% of persons

primary tuberculosis: the initial stages

• first 3 weeks of initial infection (previously unexposed person)

  • bacilli enter the airways and land in alveoli

    • upper airways most common

  • alveolar macrophages ingest bacilli

    • cellular enzymes cannot destroy the bacillus at this point because of the waxy capsule

  • bacilli replicate within macrophage

    • if client has intact immune system, infected macrophages initiate cell-mediated immunity

primary tuberculosis: cell mediated immunity (someone with strong immune system)

• after first 3 weeks

  • infected macrophages (APCs) attach TB antigen to MHC II → presentation to CD4 cells → activation of T helper cells

  • T helper cells recruit more macrophages and lymphocytes

    • formation of granuloma (tubercle) to isolate mycobacterium

    • also called a Ghon focus

      • macrophages in middle and lymphocytes on outside

  • T helper cells also reprogram infected macrophages to release stronger enzymes to destroy TB

    • enzymes destroy bacteria and lung tissue (caseous necrosis)

    • PPD is positive at this point

  • if there is a delay forming the tubercle, TB might multiply and spread from ghon focus to the regional lymph nodes

    • causes necrosis (caseous necrosis) in the hilum

    • called a ghon complex

    • ghon complex will ultimately “heal”

    • can become fibrotic or calcified

    • visible on x-ray

latent tuberculosis

• in most patients, the bacteria will go into a latent stage

  • bacteria are still viable but dormant

  • person is not infectious at this time

  • can reactivate with immunosuppression or re-exposure

secondary tuberculosis

• disease that develops in previously sensitized host due to

  • new exposure (memory cells)

  • reactivation of latent TB when immune system is down

• infection spreads to upper lobes of lung

• immune response is rapid due to previous sensitivity

• multiple areas of caseous necrosis

  • lesions can erode into airways → expel contents into airways

  • empty, calcified / fibrotic space left behind (cavitation)

    • after the lesions clear out and are exposed by you coughing, it leaves behind a hold inside your lung

  • patient develops bronchopneumonia

• TB can erode into blood vessels and spread to other organs (kidneys, meninges, liver, etc)

  • this is called miliary TB

tuberculosis clinical manifestations

• primary tuberculosis with an intact immune system

  • asymptomatic or flu-like symptoms

• secondary tuberculosis

  • fatigue

  • anorexia

  • low grade fever

  • night sweats

  • hemoptysis

  • pleuritic pain

• diagnostics

  • acid-fast bacillus

tuberculosis: weak immunity

• in someone who is immunocompromised, the bacteria can replicate and cause illness

  • 5% of persons

primary progressive tuberculosis (someone with WEAK immune system)

• the macrophages cannot contain the bacteria

  • clients progress from primary TB to clinically significant (progressive) disease immediately

  • resembles bacterial pneumonia

  • elderly and immunosuppressed are highest risk

• clinical presentation

  • fever

  • fatigue

  • weight loss

  • night sweats

• bacillus gains access to sputum - client is infectious

• bacillus can enter bloodstream and spread to other organs (miliary TB)

lung cancer

• malignancies that arise from epithelium of respiratory tract (bronchogenic carcinomas)

• 2nd most common cause of death in the US → we don’t have a good screening available

• most common cause of cancer-related death

• risk factors

  • smoking (10-15% of smokers will develop lung cancer)

  • occupational exposure to certain substances (asbestos fibers, diesel fuel, radon gas, silica, etc.)

  • genetics

lung cancer: types

• two major categories based on biopsy

  • small cell lung cancer (harder to detect)

  • non-small cell lung carcinoma (85%)

    • squamous cell carcinoma

    • adenocarcinoma

    • large cell undifferentiated carcinoma