Exam 2: Gero Lecture 6 PATHO Flashcards by Taylor Biggs

GERD etiology

older age
meds
nicotine
obesity
hiatalehemia

How well did you know this?

Not at all

Perfectly

GERD CM

dysphagia
heartburn
epigastric pain
dry cough
water brash: increase spit
laryngitis
asthma attacks

How well did you know this?

Not at all

Perfectly

GERD patho

weakened LES/ increase intra- abd pressure
stomach contents reflex up to esophagus
acidic juices irritate epithelium and erosion
repeat injury causes metaplasia of epithelial cells
barrets esophagus: esophagus cancer

How well did you know this?

Not at all

Perfectly

OP etiology

primary: postmenopausal (lose estrogen)
secondary: other condition

How well did you know this?

Not at all

Perfectly

OP CM

decrease heigh
compression spinal FX
kyphosis
decrease bone mass measurements
pathologic FX

How well did you know this?

Not at all

Perfectly

OP patho

decrease estrogen
increase RANKL
bone reabsorption is greater than bone deposition
alter in bone microarchitecture
loss of bone mineralization
diminished bone mass and porous bone

How well did you know this?

Not at all

Perfectly

what is OP?

a metabolic bone disease resulting in a reduction in density in a reduction in density or mass of bone
bone becomes lacy and weak; decrease density

How well did you know this?

Not at all

Perfectly

what is OA?

a progressive destruction of cartilage in both synovial joints and vertebrae (bone rubbing bone)

How well did you know this?

Not at all

Perfectly

OA etiology

risk factors
secondary:
age
obesity
injury
repetitive trauma
primary: idiopathic

How well did you know this?

Not at all

Perfectly

OA CM

asymmetric joint pain
increase w activity
relieved by rest
heberdens nodes (DIP)
bouchards nodes (PIP)

How well did you know this?

Not at all

Perfectly

OA patho

loss of articular cartilage
inflam response
new bone form of joint margins (bone spurs)
subchondral bone changes
synovitis and thickening of joint capsule

How well did you know this?

Not at all

Perfectly

What is RA?

a chronic progressive systemic auto immune disease with inflam of joints and deformity

How well did you know this?

Not at all

Perfectly

RA etiology

unclear
higher in women
autoimmune
most common to: OA

How well did you know this?

Not at all

Perfectly

RA CM

symmetrical pain in small joints
swelling
warmth
erythema
anorexia/fatigue
ulnar drift
swan neck deform. (finger looks like swan neck)
boutonniere deform

How well did you know this?

Not at all

Perfectly

RA patho

B lymph activation
RA factors is form and binds w IgG
inflam response
enzyme destroy collagen
forms pannus (thick abnorm. layer of grandiose tissue)
destruction of cartilage and bone
RANKL increase
T lymph activation

How well did you know this?

Not at all

Perfectly

Hyperthyroidism (thyrotoxicosis) etiology

graves disease
autoimmune
disorder/type II hypersensitivity toxic multi-nodular goiter (not common)
toxic adenoma (lump on thyroid)

Hyperthyroidism CM

weigh loss
nervousness
hyperactive reflexes
diaphoresis
tachycardia
increase SBP
expothalmus

Hyperthyroidism patho

body produces TSI or gland enlarges
increase T3 and T4
neg feedback inhibition of pituitary TSH
low TSH more hormone secreted
high basal metabolic rate

hypothyroidism etiology

congenital thyroid defects
autoimmune: Hashimoto disease (common)
surgical removal
thyroiditis

hypothyroidism CM

fatigue
weight gain
constipation
delayed reflex
feels cold
sluggishness

hypothyroidism patho

loss of thyroid function
decrease production of thyroid hormone (TH)
increase production of TSH
slow basal metabolism rate

DMT2 etiology

exact etiology Unknown

risk factors: obesity and genetics

DMT2 CM

polyuria
polydipsia
polyphagia
fatigue
pruritus
recurrent infection

DMT2 patho

genetic:
decrease activity of amylin (co-secreted with insulin)
decrease beta cell mass function
hypoinsulinemia
increase glucagon

obesity:
decrease activity of ghrelin
insulin resistance
increase demand for insulin synthesis leads to hyperinsulinemia

HIGH BS

Prostate CA etiology

dietary factors hormones: androgen chronic inflam genetic factors: BRCA2

prostate CA patho

>95% are adenocarcinomas norm/ semen secreting cells mutate to PSG/CIS to adenocarcinomas

prostate CA CM

mainly asymptomatic --> screening with DRE and PSA is key bladder outlet obstruction --> slow urine stream, hesitancy, incomplete bladder empty, frequency, nocturia, dysuria back pain --> bone metastasis

HTN silent killer etiology

primary: idiopathic secondary: underlying disorder

HTN CM

HA fatigue impaired vision decrease urine output dizzy epistaxis flushed face

HTN patho

dysfunction of SNS, RAA, and natriuretic hormones (ANA and BNP) renal Na+ and H2O retention --> inflam increase blood vol sustained HTN dysfunction of SNS, RAA, and natriuretic hormones (ANA and BNP) vasoconstriction --> obesity increase peripheral resistance sustained HTN

LHF (CHF) etiology

increase RAAS = increase aldosterone pt at risk for hypokalemia LUNGS CAD: myocardial ischemia MI cardiomyopathy HTN; pulmonary HTN valve disease CKD anemia hyperthyroidism: thyroid controls vasometabolism; severe tachycardia

LHF (CHF) CM

dyspnea orthopnea frothy sputum fatigue decrease urine output edema abnormal heart sounds (s3 gallops) pulmonary congestion

LHF patho

decrease contracting cause SV to fall and LVEDV increase -- dialation kidney sense decrease in blood flow activation of RAA increase PVR increase preload and after load increase hydrostatic pressure into pulmonary system back up fluid pulmonary edema aortic pressure fall and systemic arterial pressure decreases baroreceptors sense a decrease activates SNS and hypothalamus releases ADH

RHF etiology

rest of body LHF increase pulmonary vascular resistance ARDS COPD

RHF cm

peripheral edema ascites JVD hepatomegaly nocturia weight gain

RHF patho

lung disease increase pulmonary vascular resistance increase force of RV contraction increase RV o2 demand decrease o2 supply RV hypoxia decrease force of RV contraction increase RV preload increase RA preload edema