!!Exam 2 Patho Final Review

process of cancer development

1. initiation

2. promotion

3. progression

initiation stage of cancer development

1st stage

• alteration of DNA and unless damaged cell doesnt die or repair itself , it will replicate with same alteration

“ 1 cell gets DNA damaged and replicated”

Promotion stage of cancer development

2nd stage

• activities promoting REVERSIBLE reproduction of altered cells

• ex: smoking, obesity, alcohol, inactivity

Progression stage of cancer development

3rd stage

• increased growth rate, IRREVERSIBLE, angiogenesis, invasiveness and metastasis

Benign Tumors

• invade or metastasize?

• normal function/ structure?

• capsulated?

• recurrence or vasculature?

• differentiation?

ex- pituitary adenoma

• dont invade or metastasize

• retain normal cell function and structure

• encapsulated

• has no recurrence or vasculature

• well differentiated

Malignant Tumors

• invade or metastasize?

• normal function/ structure?

• capsulated?

• recurrence or vasculature?

• differentiation?

ex- melanoma, carcinoma

• does invade and metastasize

• does not retain normal cell function and structure

• not encapsulated

• has recurrence and vasculature

• poorly differentiated

cancer classification

• location, origin

• tumor node metastases (TNM)

• histology

• staging

Tumor Node Metastases

• T: size and invasiveness 

  • T1 (small) - T4 (large)

• N: node involvement

  • N1 (local)- N4 (wide spread of nodes)

• M: metastases (spread) 

  • 0 (hasnt spread) or 1

histology classification or cancer cells

• differ/abnormalities?

• dysplasia?

• differentiation?

• grade 1: cells differ slightly (mild dysplasia) and are well differentiated (low grade)

• grade 2: cells are more abnormal (moderate dysplasia) and moderately differentiated (intermediate grade)

• grade 3: cells are very abnormal (severe dysplasia) and poorly differentiated (high grade)

• grade 4: cells are immature, primitive (anaplasia) and undifferentiated (high grade)

• grade 5: grade cannot be assessed

Staging classification of Cancer

(can never decrease but can increase in stage)

• 0: in situ (local, no apparent tendency to grow or metastasize

• 1: limited to tissue of origin

• 2: limited local spread

• 3: extensive local and regional spread

• 4: metastasis

tumor lysis syndrome

pre cancerous skin conditions (non melanoma)

• #1 causative agent

• where?

• types

sun exposure = #1 causative factor

• likely found in face, head, neck, back of hands, and arms

Basal Cell carcinoma, Squamous cell carcinoma, Acticin Keratosis

• pre malignant skin lesions

• impossible to distinguish between AK and squamous cell 

• biopsy a nd treat

Basal Cell Carcinoma

(non melanoma precancerous skin condition)

• most common type of skin cancer

• maybe in areas of body that were NOT sun exposed

• least deadly rarely metastasizes

• nodular of ulcercative depression in the center of eryhtematous and pearly

• treat with removal, laser, FLUOROUACIL

squamous cel carcinoma

• contributions

• treatment

potential to metastasize

• immunosuppression leads to dramatic increase in incidence

• smoking contributes to formation on mouth and lips

• thin, scaly, erythematous progresses to have firm nodules and sales and horns

• treat with removal, radiation, FLUOROURACIL, chemo for mets

Malignant Melanoma

cause unknown

• incidence increasing

• can metastasize to any organ

• 5 year survival rate with advanced disease <10%

Bacterial Skin Infections

• carbuncle

• cellulitis

• Erysipelas

• Folliculitis

• Furuncle

• Impetigo

Viral Skin infections

• herpes simplex 1 & 2

• herpes zoster

• plantar warts

• verruca vulgaris

Fungal Skin Infections

• Candidiasis (yeast infection)

• tinea corporis (ring worm)

• tinea cruris (jock itch)

• tinea pedis (athletes foot)

• Tinea Uguium (onchomycosis)

cutaneous Drug Reactions

steven johns syndrom (SJS)/ Toxic Epidermal Necrolysis (TEN)

• violent immune response 4-21 days after starting use of offending drugs

• priority: stop drug

• supportive care

Most common drugs: SATAN

• sulfa, allopurinal, tetracyclines, anticonvulsants, NSAIDs

Infestations

??

Hypovolemia

causes

• GI loses

• inadequate intake

• burns, shock, blood loss

manifestation

• increased HR, low BP

• dry mucous membranes

• decreased OUP, prolonged cap refill

Hypervolemia

causes

• renal/heart failure

• excessive fluid administation

manifestation

• increase HR and BP

• bounding pulse, jugular vein distention

• edema, crackles

• cough, confusion

Hyponatremia

causes

• excessive free water intake

• diuretic drugs

• GI losses

• SIADH, addisons

Manifestation

• confusion (coma, death)

• seizures, N/V/D

Hypernatremia

causes:

• sweating and dehydration

• fever

• exercise

• hypertonic fluid administration

• diabetes

manifestations

• confusion (coma, death)

• seizures

• intense thirst

Hypocalcemia

causes

• hypoparathyroidism

• CKD

• tumor lysis syndrome

• pancreatitis

• insufficient intake

Manifestations

• laryngeal sprasm/stridor

• tetant

• arrythmias, seizures

• positive trousseau’s and chovstek signs

• weak bones

• diarrhea

Hypercalcemia

causes

• cancer (1/3)

• hyperparathyroidism (2/3)

manifestations

• kidney stones

• fatigue

• bone pain

• constipation

Hypokalemia

causes

• non potassium sparing diuretic

• GI losses

manifestations

• flattened T waves, Big U waves

• muscle weakness

• constipation

• confusion

Hyperkalemia

causes

• renal failure

• crush injuries

• excessive potassium supplementation

manifestations

• tall T waves

• irritability or confusion

• muscle weakness

Hypomagnesemia

causes

• alcohol use disorder, malnutrition/malabsorption

manifestations:

• muscle spasms

• hyperactive reflex

• torsades de pointes

Hypermagnesemia

causes

• renal failure

• excessive mag intake

manifestations

• muscle weakness (inclusing respiratory muscles)

• hypoactive reflexes

• diarrhea

• confusion

Respiratory acidosis causes and compensation

causes

• hypoventilitation

• respiratory failure

compensation

• kidney converse HCO 3 and secrete H into urine

respiratory acidosis manifestations

decreased BP
- rapid, shallow breaths
- hyperkalemia
- muscle weakness
- dizziness, disorientation

respiratory alkalosis causes and compenstion

causes

• hypoxemia from acute pulmonary disorders

• hyperventilation (pain, anxiety, CNS disorders)

• mechanical ventilation

compensation

• Kidneys will excrete more HCO3 so it is more acid, OR retain more H+

Respiratory Alkalosis Manifestation

decreased BP
- seizures
- light headedness
- hypokalemia
- tachycardia
- N/V

• numbenes and tingling of extremities

Metabolic Acidosis causes and compensation

causes

• ketoacidosis

• lactic acid accumulation (shock),

• severe diarrhea

• kidney disease

compensation

• increased CO2 excretion (Kussmaul resp) and kidneys secrete acid

Metabolic Acidosis Manifestations

decreased BP
- headache
- changes in LOC
- hyperkalemia
- cool, clammy skin

N/V/D

muscle twitching

Metabolic Alkalosis causes and compensation

causes

• prolonged vomiting

• excessive gastric suctioning

• diuretics

compensation

• renal excretion of HCO3

• hypoventilation

metabolic alkalosis manifestations

restlessness followed by lethargy
- confusion
- NVD
- dysrhythmias
- tremors, peripheral neuropathy
- hypokalemia

Lower UTI Manifestations

almost 50% of all patients have no symptoms 

• burning upon urination (cystitis)

• urgency frequency (>every 3 hours)

• nocturia

• urinary incontinence

• supraprubic pain

• hematuria

• back pain

UTI treatment

• urinary analgesic: Phenaxopyridine (doesnt actually treat infections)

  • available OTC and inform pt (urine turns orange/ red color)

• fungal: fluconazole

Pyelonephritis

infection ascends to kindeys

• UTI symptoms + flank pain with CVA tenderness

• signs of systemic infections: fever/ chills, N/V, malaise

• may need inpatient treatment

• can lead to renal failure if untreated

• Manifestations: systemic symptoms and lower UTI symptoms may still be present 

• increase risk in pregnancy (can lead to miscarriage)

Pyelonephritis Treatment (mild symptoms)

• mild symptoms: output or short input

  • fluids, NSAIDs, antipyretics, follow cultures and imaging

  • ABX: broad spectrum (Fluroquinolone PO), 7-21 days, depending on severity, sensitivity guided (definitive ABX)

Pyelonephritis Treatment (severe symptoms)

• IV fluids until oral tolerated

• parental antibiotics (ceftriaxone, Fluroquinolone, or comb therapy)

Immunologic Disorders: Glomerulonephritis

inflammation of Gomeruli

• tubular and interstitial changes

• vascular scarring, hardening= glomerulosclerosis

• affects BOTH kidneys

• 3rd leading cause of ESRD in US

• acute and chronic types

Acute Poststreptococcal Glomerulonephritis

• MOA unknown

• common in children, young adults, older adults

• develops 1-2 weeks after group A-B hemolytic streptococcal infections

  • tonsils, pharynx

  • resp tract

  • skin

• Immunologic Response from kidneys after infection (didnt travel from throat to kidneys)

Chronic Glomerulonephritis

• permanent and progressive renal fibrosis

• can progress to ESRD

• may be asymptomatic and unaware

Management: treat underlying cause and supportive care

• land lead to nephrotic syndrome 

Urinary tract Calculi (renal colic) 

• Nephrolithiasis= kidney stone (renal colic) disease

• concentration of supersaturated crystals precipitate and form stones

• RISKS:

  • middle aged and older adults, caucasion, family history, hot climates, dehydration

Renal Colic Manifestations

• sudden, severe , wave like colicky pain

• flank, pain, back or lower abdomen

• caused by ureter stretching, dilating, and spasming

• M/V common

• “kidney stone dance”

• with infection: dysuria, fever, chills

Renal Colic Medication Management

• pain relief

  • opioids

  • NSAIDs

  • alphodrenergic blockers (flomax)

• adequate hydration, dont over do it could lead to increase urination leading to more pain

Acute Kidney Injury (AKI)

• new and rapid/ continuum

• slight deterioration—> severe impairment

• rapid loss of renal function

• high mortality rate

• potentially reversible

AKI: diagnostic tests:

• increase in serum creatinine and/or reduction in urine output

  • increase in creatinine greater/equal to 0.3 mg/dL within 48 hours

• increased BUN and potassium K

• Azotemia= accumulation of nitrogenous waste products in the blood

Prerenal AKI

• causes lead to reduced systemic circulation resulting in decreased renal blood flow

  • EX: blood loss, burn victim, anaphylaxis, hypotension, hypoperfusion

• does NOT involve damage to renal tissue directly

• Result: decreased sodium excretion and decreased urine output, increased sodium and water retention

Intrarenal AKI

• caused by conditions that cause direct damage to kidney tissue

  • EX: prolonged ischemia, nephrotoxins (ABX: gentamicin, vancomycin and NSAIDs)

    • contrast dye and media

    • hemolyzed RBCs ( type 2 sensitivity)

    • Rhabdomyolysis (overexercising)

    • Kidney diseases (acute glomerulonephritis and systemic lupus erythematosus)

  • poor perfusion and low O2

Postrenal AKI

• cause: obstruction of outflow leads to reflux into the renal pelvis

• can lead to hydronephrosis (swollen kidney/s)

• EX: benign prostatic hyperplasia, prostate cancer, calculi, trauma, extrarenal tumors

AKI Phases

• Oliguria: day 1 to 10-14: 

  • starts 1-7 days after injury, last approx 10-14 days (maybe a month)

• Diuretic: 1-3 weeks

• Recovery: up to 12 months

AKI Phase: Oliguria

• 1-7 days after injury and last 10-14 days

• 50% of patients are asymptomatic with normal urine output

• Symp: urine output , 400 mL/day (normal=30mL/hr)

• Hypervolemia

• expected manifestations: edema, crackles, bounding pulse, HF

• Metabolic acidosis, increased serum creatinine

AKI Phase: Oliguria, Urinalysis Findings

• protein

• casts (slough): sign of decreased glomerular filtration, formed when materials solidify and take the shape of the kidney tubules

  • tiny, tubed shape particles

  • Types: RBCs and WBCs, Muddy brown (acute tubular necrosis), epithelial cells

AKI Phase: Oliguric Medications

• supportive care to manage symptoms

• diuretic medications

• Potassium lowering meds— may require dialysis

AKI Phase: Diuretic

• last 1-3 weeks

• dramatic increase in urine output: 1-5 L/day

• cause: from high urea and inability uf tubules to concentrate urine

• Risks: hypovolemia, hypotension, dehydration, hyponatremia and hypokalemia

• monitor I/O, electrolytes

• Manifestations: metabolic acidosis

AKI Phase: Recovery

• last up to 1 year

• begins when GFR starts to increase (increasing continues)

• decreased BUN and decreased Creatinine

• amount of recovery depends on: severity of injury, complications, comorbidities

• some never recover— progress to ESRD

Chronic Kidney Disease CKD

• progressive, irreversible loss of kidney function

• many are asymptomatic and unaware=untreated

• high mortality without transplant or dialysis

• Leading causes: diabetes (50%), Hypotension (25%)

CKD Diagnosis

• GFR <60 for 3 months or longer

• ESRD= GFR 15

stages of CKD

stage 5= GFR <15

CKD Manifestations

• systemic

• decreased GFR

• increased BUN and creatinine

• hyperkalemia, hyperphosphatemia, hypermagnesemia

• hypocalcemia

• anemia

• eremic fetor, ammonia odor breath

• periphera neuropathy

CKD imbalances

• decreased GFR, increased BUN, increased creatinine

• increased K hyperkalemia: most serious imbalance can be fatal

• decreased Ca hypocalcemia

• hyperphosphatemia and hypermagnesemia