Exam 2: Gero Lecture 6 PATHO Flashcards
GERD etiology
older age
meds
nicotine
obesity
hiatalehemia
GERD CM
dysphagia
heartburn
epigastric pain
dry cough
water brash: increase spit
laryngitis
asthma attacks
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
OP etiology
primary: postmenopausal (lose estrogen)
secondary: other condition
OP CM
decrease heigh
compression spinal FX
kyphosis
decrease bone mass measurements
pathologic FX
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
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
what is OA?
a progressive destruction of cartilage in both synovial joints and vertebrae (bone rubbing bone)
OA etiology
risk factors
secondary:
age
obesity
injury
repetitive trauma
primary: idiopathic
OA CM
asymmetric joint pain
increase w activity
relieved by rest
heberdens nodes (DIP)
bouchards nodes (PIP)
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
What is RA?
a chronic progressive systemic auto immune disease with inflam of joints and deformity
RA etiology
unclear
higher in women
autoimmune
most common to: OA
RA CM
symmetrical pain in small joints
swelling
warmth
erythema
anorexia/fatigue
ulnar drift
swan neck deform. (finger looks like swan neck)
boutonniere deform
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
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
