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Pathophysiology, Pharmacology, and Therapeutics > Exam 4 Concepts > Flashcards

Exam 4 Concepts Flashcards

1
Q

dumping syndrome

A

pyloric sphincter does not work

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2
Q

surface mucous cell

A

secretes mucous

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3
Q

mucous neck cell

A

secretes mucus

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4
Q

parietal cell

A

secrets hydrochloric acid and intrinsic factor

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5
Q

chief cell

A

secretes pepsinogen and gastric lipase

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6
Q

G cell

A

secretes the hormone gastrin

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7
Q

where does gastric acid come from?

A

secreted by parietal cells at basal rate and in response to stimuli

via proton pump (H+-K+ pump aka gastric pump)

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8
Q

how does proton pump work?

A

moves H+ ion out of parietal cell and into stomach lumen and K+ ion back into cell AGAINST concentration gradients (splits ATP)

Cl- also moves into stomach to form HCL with H+

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9
Q

what stimulates acid secretion beyond basal secretion

A

gastrin
acetylcholine
histamine

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10
Q

H2 receptor

A

G Protein-Coupled receptor (GPCR)

  • histamine binds, activating alpha subunit of G protein
  • subunit dissociates and binds to AC
  • AC converts ATP to cAMP
  • protein kinase A activated and phosphorylates proteins that transport H/K pump to plasma membrane
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11
Q

LES normal tone

A

LES is normally a high pressure zone with pressure exceeding intragastric pressure

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12
Q

acid disorders result from…

A

imbalance of aggressive/damaging factors and mucosal defense factors

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13
Q

mucosal resistance

A

mucus layer + HCO3-

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14
Q

gastric empyting

A

moves substances along and sweeps away H+ ions that might leak through

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15
Q

epidermal growth factor

A

ensures rapid turnover of epithelial cells, enhancing repair of any damage to the epithelium - wounds heal quickly

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16
Q

maintaining the integrity of the gastric mucosal barrier

A
  • HCO3-
  • pH of mucosa = 7; pH of lumen = 2
  • mucous cells = physical barrier; release mucus
  • mucin proteins to maintain barrier fxn
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17
Q

mucins

A

large, heavily glycosylated proteins which gives them a high degree of water-holding capacity and resistance to proteolysis

sticky, hold together - form gel-like barrier

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18
Q

GERD

A

gastroesophageal reflux disease

symptomatic condition or histologic change associated w/ retrograde movement of gastric contents to esophagus

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19
Q

PUD

A

peptic ulcer disease

gastritis, erosions, ulcers of GI tract that require gastric acid for formation

duodenal ulcers more common than stomach ulcers

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20
Q

most common cause of GERD

A

incompetent LES - allows acid reflux

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21
Q

LES

A

lower esophageal sphincter

high-pressure zone of thickened muscle between esophagus and stomach. works in concert w/ diaphragm to prevent reflux

normally 15-30 mmHg above intragastric pressures

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22
Q

other causes of GERD

A

anything that alters normal fxn and/or tone of LES OR increases abdominal pressure

certain foods/meds
smoking
obesity
hiatal hernia
pregnancy
sleeping positions
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23
Q

hiatal hernia

A

stomach bulges up into chest through opening where esophagus passes through diaphragm

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24
Q

sliding hiatal hernia

A

stomach and section of esophagus that joins stomach slides up chest through hiatus

more common

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25
Q

paraesophageal hernia

A

stomach squeezed through hiatus and next to esophagus - stomach can become incarcerated and blood supply cut off

more dangerous

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26
Q

peppermint

A

relaxes LS (carminative)

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27
Q

calcium channel blockers

A

relaxes muscles (esophageal sphincter)

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28
Q

cigarette smoke

A

direct esophageal irritant

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29
Q

typical GERD symptoms

A 
heartburn in sternum
water brash (hypersalivation)
belching
regurgitation w/w/out nausea
worse when supine
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30
Q

complication symptoms of GERD

A 
continual pain
dysphagia
odynophagia (pain)
vomiting acid in sleep
bleeding
unexplained weight loss
choking
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31
Q

atypical (extra-esophageal) symptoms

A 
non-allergic asthma
chronic cough
hoarseness
laryngitis
chest pain
dental erosions
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32
Q

Barrett’s esophagus

A

metaplasia due to chronic exposure to gastric acids

stratified squamous replaced by columnar w/ goblet cells - more likely to develop adenocarcinoma

pts. need monitoring

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33
Q

GERD complications

A

delayed gastric emptying

increased frequency of transient LES relaxations

increased acidity

loss of secondary peristalsis following transient LES relaxations

decreased LES tone

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34
Q

common causes of PUD

A

helicobacter pylori infection
NSAIDS
smoking increases risk

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35
Q

characteristics of H.pylori

A

G-
slow-growing
flagella to move below mucosal surface

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36
Q

how H.pylori infection can lead to PUD

A

well-adapted to gastric environment - lives w/in or beneath gastric mucosal layer

disrupts mucosal layer, neutralizes pH (mucin degels), releases enzymes and toxins, adheres to gastric epithelium

promotes inflammatory rxn and inhibits apoptosis of host cell

mucosal disruption leads to tissue injury, erosion, ulcer

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37
Q

H.pylori flagella in mucosal injury

A

bacterial mobility and chemotaxis to colonize under mucosa

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38
Q

H.pylori urease in mucosal injury

A

neutralize gastric acid

gastric mucosal injury via ammonia

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39
Q

H.pylori lipopolysaccharides in mucosal injury

A

G-
adhere to host cells
inflammation

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40
Q

H.Pylori outer proteins in mucosal injury

A

adhere to host cells

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41
Q

H.Pylori effectors in mucosal injury

A

actin remodeling

Il-8: pro-inflammatory, host cell growth, inhibits apoptosis

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42
Q

H.pylori secretory enzymes in mucosal injury

A

mucinase, protease, lipase: gastric mucosal injury

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43
Q

H.pylori type IV secretion system in mucosal injury

A

pilli-like structure for injection of effectors

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44
Q

diagnosing H.pylori infection

A

biospy via endoscopy = gold standard

H.pylori breath test - non-invasive and reliable

H.pylori serum antibodies sometimes measured, but not recommended for diagnostic purposes

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45
Q

H.pylori breath test

A
  • H.pylori releases urease which breaks urea down into CO2 and ammonium
  • carbon-12 more abundant than carbon-13
  • pre/post test with liquid urea from carbon-13
  • 13C-urea broken into 13CO2 and NH4 if H.pylori is present
  • 13CO2 absorbed into stomach, bloodstream, and exhaled out lungs

pre and post ratios of 13CO2 and 12CO2 measured - increased ratio means H.pylori

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46
Q

NSAIDs can cause PUD

A

long-term/high-dose therapy

direct topical injury to gastric mucosa

increased neutrophil adherence to vascular endothelium –> neutrophil-derived ROS and proteases –> damage to mucosal layer

inhibit beneficial prostaglandins

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47
Q

prostaglandin inhibition in PUD

A

decreased submucosal blood flow - ischemia

decreased mucosal proliferation

decreased production of mucus and bicarb (allows erosion in presence of HCl)

increased secretion of gastric acid and pepsin

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48
Q

risk factors for NSAID-induced PUD

A 
>65
previous Hx of PUD
combined NSAIDS
combo with corticosteroids
smoking
heavy alcohol consumption
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49
Q

stress uulcer prophylaxis

A

71% of pts on gen med units receive acid-suppressing therapy without an appropriate indication

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50
Q

stress ulcer prophylaxis recommended in ICU pts. with following symptoms:

A 
coagulopathy
prolonged ventilation
GI ulcer/bleeding in past yr
sepsis
>1 week in ICU
occult GI bleeding > 6 days
steroid therapy > 250mg daily
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51
Q

PUD symptoms

A 
general, mild epigastric pain
nausea
food aggravates gastric pain
food relieves duodenal pain
may be asymptomatic
anemia w/ bleeding
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52
Q

PUD complications

A

bleeding: black/tarry stools or hematemesis (coffee ground)

perforation

obstruction

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53
Q

non-pharmacologic approaches for GERD and PUD

A

lifestyle (GERD)
discontinue NSAIDS (PUD)
surgery

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54
Q

GERD lifestyle modifications

A

elevate head of bed

dietary changes: avoid certain foods, eat small meals, avoid eating w/in 3 hrs of laying down

weight reduction if appropriate

stop smoking/drinking

avoid tight-fitting clothes

discontinue meds that exacerbate

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55
Q

oral regimens to eradicate H.pylori-induced PUD

A

PPI and 2 antibiotics

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56
Q

1 and #2 cause of ESRD

A 
#1: diabetes
#2: hypertension
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57
Q

proper kidney fxn: set body fluid volume and composition

A

maintain stable volume and composition of body fluids

reabsorb filtered nutrients (glucose, amino acids)

retain blood cells/proteins in bloodstream, and not leak into urine

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58
Q

composition of body fluids balanced by kidney

A 
water
sodium
potassium
calcium
phosphorus
acid/base
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59
Q

kidney excretion of wastes

A

creatinine
urea

metabolic end products of drugs and hormones (liver conjugation –> water soluble)

acid (meat consumption)

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60
Q

creatinine

A

product of muscle metabolism

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61
Q

urea

A

product of amino acid metabolism

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62
Q

endocrine fxns of kidneys

A

erythropoietin

Vit. D conversion to active form

Renin

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63
Q

erythropoietin

A

RBC growth factor
release stimulated by hypoxia

binds with receptors in bone marrow to stimulate production of RBCs

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64
Q

Vitamin D conversion to active form

A

kidney performs second hydroxylation of vitamin D to form active form of Vit. D necessary for calcium absorption

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65
Q

renin

A

regulates blood volume and blood pressure via renin-angiotensin-aldosterone system

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66
Q

renal blood flow

A

kidneys = 1% body mass

receive 20-25% CO

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67
Q

normal glomerular filtration rate

A

125mL/min

actual rate of urine production = 1.5 L/day

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68
Q

nephron structures

A 
glomerulus
PCT
loop of Henle
DCT
collecting tubule
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69
Q

juxtamedullary nephrons

A

loop of Henle extends through cortex into medulla

low blood flow - vulnerable to ischemia

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70
Q

glomerulus

A

site of filtration from blood

formed by glomerular capillary tuft, podocytes of Bowman’s capsule, basement membrane

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71
Q

basement membrane and proteins in slit pores of podocytes

A

prevent passage of cell snad large proteins

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72
Q

mesangial cells

A

in basement membrane of glomerulus

structural support for glomerular capillaries, secretion of matrix proteins, phagocytosis, regulate GFR

by contracting/relaxing, mesangial cells alter available surface area for filtration and affect GFR

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73
Q

mesangium

A

mesangial cells + mesangial matix

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74
Q

mesangial cells in diabetic-induced CKD

A

become fibrotic so they can’t contract and relax anymore

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75
Q

filtration through glomerulus

A

10% renal blood flow leaves circulation and enters glomerular space via glomerular filtration

fluid = ultrafiltrate of plasma (water, ions, small molecules, a.a, urea, creatinin, drugs, hormones)

blood cells/proteins retained in bloodstream

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76
Q

negative charges in basement membrane and podocytes

A

repel proteins

key factor in glomerulus ability to prevent plasma proteins leaking into urine

remaining tubular structures process fluid and return 99% water/substances back to circulation

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77
Q

steps in glomerular filtration

A
  1. glomerular filtrate leaves vascular space, enters urine at glomerular capillaries
  2. water, electrolytes, glucose, others substances reabsorbed by renal tubules and return to circulation by peritubular capillaries
  3. remaining fluid is hypertonic
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78
Q

GFR overview

A

gold standard method of expressing kidney fxn

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79
Q

how can glomerular capillaries have such a high filtration rate relative to other systemic capillaries?

A

high glomerular hydrostatic pressure (pushing force for fluid)

glomerular capillaries have high surface area and high permeability. highly fenestrated (50X more permeable than muscle capillaries).

glomerular capillaries, basement membrane, podocytes, allow filtration: movement of water/small solutes but RESTRICT protein movement from blood to Bowman’s space

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80
Q

regulation of GFR

A

proportional to number of nephrons - declines w/ age

proportional to renal blood flow

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81
Q

mechanisms of kidney injury

A

acute, often reversible injury (such as nephrotoxic antiboitic drugs) vs. chronic injury

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82
Q

glomerular abnormalities (acute or chronic)

A

sclerosis of glomerular basement membrane

scarring and deposit of immune complexes (infection, SLE)

loss of basement membrane negative charges that normally repel protein filtration

effacement of podocytes (change in morphology - thin and narrow)

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83
Q

tubular injuries

A

more common in acute kidney injury

ischemic insult to deep medullary interstitium

increased vulnerability to ROS

hyperfiltration, particularly with protein leakage

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84
Q

causes of glomerular scarring and injury

A

deposition of immune complexes and antibodies in interstitium due to:

  • strep
  • viral infections
  • systemic lupus erythematosus
  • IgA nephropathy
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85
Q

loss of nephrons to diseae =

A

loss of GFR

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86
Q

DM in ESRD

A

chronic hyperglycemia leads to hyperfiltration and increased albumin excretion
-hyperfiltration becomes source of injury

hyperglycemia modifies endothelial cell properties and proteins in glomerular basement membrane, altering structure and fxn of filtration barrier

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87
Q

various processes contribute to excessive vascular leakiness in kidneys

A

ROS damage and inflammation damage endothelium

basement membrane becomes thickened, sclerotic, loses (-) charge

podocytes effaced, lose interlocking characteristic

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88
Q

hypertension in ESRD

A

arteriosclerosis of small arteries and arterioles

-reduced renal blood flow, glomerular scarring

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89
Q

measurement and estimation of GFR

A

Modification of Diet in Renal Disease (MDRD)

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90
Q

serum creatinine

A

normally freely filtered in glomerulus and excreted in urine at constant rate
-dependent on muscle mass and GFR

decease in GFR, decrease creatinine excretion
-serum creatinine increases because it’s not being excreted

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91
Q

urea as marker of renal fxn

A

end-product of protein metabolism

BUN (blood urea nitrogen) can vary with hydration status and renal fxn
-looked at relative to changes in creatinine (less specific marker)

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92
Q

albuminuria as marker of renal fxn

A

albumin leaks through when glomerular barrier loses integrity

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93
Q

definition of CKD

A

abnormalities of kidney fxn for >3 months, with implications for health, including either:

  • marker of kidney damage
  • decreased GFR
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94
Q

markers of kidney damage

A 
albuminuria
urine sediment abnormalities
electrolyte/other abnormalities
histological evidence of abnormality
imaging evidence of abnormality
history of kidney transplant
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95
Q

CKD on a continuum

A
  • normal
  • increased risk
  • damage
  • decreased GFR
  • kidney failure
  • death
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96
Q

concomitant diseased with CKD

A

16-40X more likely to die of other diseases (esp. CVD) than progress to kidney failure

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97
Q

Stage 1 CKD by eGFR

A

eGFR > 90

normal or high GFR

(kidney failure if other marker of abnormality)

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98
Q

Stage 2 CKD by eGFR

A

eGFR 60-89

mildly decreased GFR

(kidney failure if other marker of abnormality)

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99
Q

Stage 3a CKD by eGFR

A

eGFR 45-59

mildly/moderately decreased GFR

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100
Q

Stage 3b CKD by eGFR

A

eGFR 30-44

moderately/severely decreased GFR

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101
Q

Stage 4 CKD by eGFR

A

eGFR 15-29

severely decreased

102
Q

Stage 1 CDK by albuminuria

A

ACR (albumin to creatinine ratio)

103
Q

Stage 2 CDK by albuminuria

A

ACR 30-300

moderately increased

104
Q

Stage 3 CDK by albuminuria

A

ACR > 300

severely increased

105
Q

major consequences of CKD

A 
hypertension
anemia
metabolic acidosis
bone disorders
CVD
106
Q

hyperphosphatemia and hypocalcemia in CKD

A

phosphorous and calcium can bind together and form a complex (also bound in bone)

hyperphosphatemia –> hypocalcemia

urinary excretion of phosphorus is impaired, so calcium binds to phosphorus in gut and is excreted, and causes calcification in soft tissues (vascular calcification)

impaired Vit. D activation –> decreased calcium absorption

hypocalcemia and decreased Vit. D activate parathyroid glands which mobilize calcium from bones via parathyroid hormone (PTH)

107
Q

CKD-MBD

A

chronic kidney disease - mineral and bone disorder

CVD greatly increases risk of cardiovascular disease

108
Q

clinical presentation of nephron loss in CKD, stages 1-3

A

fluid and electrolyte imbalance (hypertension)

anemia (seen in all stages as CKD progresses)

109
Q

clinical presentation of stages 4/5

A

severe fluid and electrolyte imbalance with elevated creatinine and BUn

hyperkalemia, hyperphosphatemia, hypocalcemia, metabolic acidosis

hypertension, CHF, PE

hypoalbuminemia

110
Q

what is the effect of hypoalbuminemia on capillary colloid osmotic pressure?

A

less albumin in blood causes decreased capillary colloid osmotic pressure. This will cause an increase in edema because fluid is being held in blood vessels, which eventually leaks out.

111
Q

major causes of death in CKD

A

MI
stroke
PVD (vessel calcification, hyperlipidemia)

112
Q

clinical presentations of CKD

A 
blood abnormalities
hormone imbalances
bone disease
neuromuscular abnormalities
GI abnormalities
skin abnormalities
113
Q

anemia in CKD results from:

A

deficiency erythropoietin
decreased RBC lifespan
nutritional deficiencies (iron, b12, folate)
dialysis-related blood loss and hemolysis

FATIGUE

114
Q

principles of CKD nonpharmacologic management

A

manage diabetes/hypertension via lifestyle changes

avoid nephrotoxic agents

medical nutrition therapy

  • decreased protein intake
  • decreased Na, K, phosphate
  • Vit. D and Ca supplementation
  • Iron/B12 reduce nutritional sources of anemia
115
Q

renal replacement therapy

A
  • discussion occur during late stage 4 CKD to determine method of RRT and create vascular access
  • not a strict numeral cut-off point for RRT
116
Q

hemodialysis

A

2/3 pts with end stage renal disease

passes through semipermeable membrane from dialysis fluid

dialysis fluid composition set to correct electrolyte imbalances and remove wastes

heparin used to prevent clotting

patients tired by next appointment because toxins have been building up over the past few days

117
Q

arteriovenous anastomosis

A

A-V fistula: artery and vein joined. vein thickens over time due to increased pressure flowing backward

most common vascular access procedure

118
Q

arteriovenous graft

A

A-V graft: artificial graft put in between vein and artery

more problems with clotting and infection

119
Q

peritoneal dialysis

A

individual’s peritoneal membrane serves as semipermeable membrane

dialysis fluid instilled in abdomen via implanted catheter; drained and replaced after time delay

cycle repeats several times a day

can be done at home or during sleep

120
Q

renal transplantation

A

first and most common organ to be transplanted

living or cadaver donors

blood typing/tissue typing done in advance of living donor

check for antibodies in recipient that may react with donor cells (negative crossmatch)

121
Q

principles of pharmacotherapy for CKD

A

prevent progression

management of complications

122
Q

anemia correction

A

iron supplementation therapy to bind oxygen, maintain adequate iron stores, promote response of erythropoietin

hematopoietic agents: promote RBC production
-requires adequate iron, B12, folate

123
Q

phosphate binders

A

MOA: reduce intestinal absorption of dietary phosphate (from proteins) by binding to phosphate in intestinal lumen

two kinds:

  1. calcium-based: calcium carbonate and calcium acetate
  2. calcium-free: sevelamer HCl and sevelamer carbonate and lanthanum carbonate
124
Q

neuropharmacologic medications

A

alter axonal conduction

alter synaptic transmission

125
Q

axonal conduction medications

A

less common

not selective; impulse is same in all neurons

126
Q

synaptic transmission medications

A

most common

can be selective; different transmitters and receptors

work by influencing receptor activity on target cells

127
Q

steps in synaptic transmision

A
  1. synthesis of transmitter
  2. storage of transmitter
  3. release of transmitter
  4. action at receptor
  5. termination of transmission
128
Q

synthesis of transmitter

A

from precursor molecules

129
Q

storage of transmitter

A

in vesicles

130
Q

release of transmitter

A

action potential causes vesicles (via Ca-gated channels) to discharge contents into synaptic cleft

131
Q

action at receptor

A

transmitter binds (reversibly) to its receptor on postsynaptic cell to illicit a response

132
Q

termination of transmission

A

transmitter dissociates from receptor and is removed by:

a) reuptake into nerve terminal
b) enzymatic degradation
c) diffusion away from gap

133
Q

reuptake of NT

A

most common

secondary active transport - sodium down its concentration gradient moves NT against its concentration gradient back into presynaptic terminal
-store or broken down

134
Q

class of neurotransmitter receptors

A

ionotropic receptors

metabotropic receptors

135
Q

ionotropic receptors

A

NT binding directly opens ion channel and changes postsynaptic membrane potential

rapid signaling

136
Q

metabotropic receptors

A

NT binding activates G protein, resulting in 2nd messenger production and/or ion channel opening

slower signaling

137
Q

characteristics of ionotropic receptors

A

ligand-binding site for NT
central pore w/ ion selectivity
rapid activation

ability to rapidly change membrane potential to depolarize (EPSP) or hyperpolarize (IPSP)

138
Q

EPSP

A

excitatory postsynaptic potential

sodium or calcium movement into cell via ionotropic receptors causes depolarization (membrane closer to or at threshold)

principal NT: gluatamte

139
Q

IPSP

A

inhibitory postsynaptic potential

potassium/chloride movement into cell via ionotropic receptors causes hyperpolarization (membrane further from threshold)

principal NT: GABA

140
Q

characteristics of metabotropic receptors

A

7 membrane-spanning regions (serpentine regions)

G-protein coupled receptors w/ NT binding site

work thru enzymes that generate 2nd messengers

G proteins can directly couple to ion channels

slower changes in membrane potential (depol. or hypol.)

can produce intracellular changes (ex: altered gene expression) - slow

141
Q

modes of neurotransmission

A

fast - ligand-operated

slow - intracellular 2nd messengers

142
Q

“fast” neurotransmitters

A

glutamic acid
ACh
GABA
glycine

143
Q

“slow” neurotransmitters

A

biogenic amines

peptides

144
Q

types of neurotransmitters

A

amino acids
amines
others

145
Q

amino acid NTs

A

glutamate (excitatory)
GABA (inhibitory)

mainly ionotropic
direct actions w/ purposeful activity
all brain regions
drugs may have widespread effects

146
Q

amine NTs

A 
dopamine
norepinephrine
serotonin
ACh (sometimes)
others
mainly metabotropic
slow, modulatory, widespread activity
discrete brain cell clusters
axons spread through CNS
drugs may act on behavior, sleep, appetite, mood, emotions
147
Q

glutamate

A

principal excitatory transmitter - most of the rapid transmission (sensory, motor, vision, hearing, consciousness)

receptors: AMPAr, NMDAr

contributes to learning/memory via NMDAr

converted to glutamine by glial cells after reuptake - sent to presynaptic terminal (or repackaged into vesicles at presynaptic terminal)

148
Q

GABA

A

synthesized from glutamate

principal CNS inhibitory NT

149
Q

GABA receptors

A

GABAa - ionotropic/ligand-gated

GABAb - metabotropic

both produce IPSPs (inhibitory)

150
Q

GABAa

A 
GABA binds to receptor
chloride channel opens
Cl flows in
hyperpolarization
decreased ability to fire
inhibitory
151
Q

acetylcholine

A

first NT identified (peripheral nervous system)

NT of:

  • all motor neurons
  • all autonomic preganglionic neurons (parasymp. and symp)
  • parasympathetic postganglionic neurons
  • a few sympathetic postganglionic neurons (sweat glands)
152
Q

acetylcholine synthesis

A 
choline + acetyl COA
--(CAT)-->
acetylcholine
--(AChe)-->
choline + acetic acid
153
Q

CAT

A

choline acetyltransferase

synthetic enzyme

154
Q

AChE

A

acetylcholinesterase

inactivation enzyme

155
Q

cholinergic neurotransmission

A

ACh uses enzymatic breakdown for NT termination

ACh binds with its receptors - degraded by acetylcholinesterase

choline returned to presynaptic nerve terminal for re-synthesis

156
Q

major central cholinergic neurons

A

basal forebrain
basal ganglia
brainstem pedunculopontine nucleus

157
Q

basal forebrain

A

central cholinergic neuron

learning, waking

nucleus basalis of Meynert degenerates in Alzheimer’s

158
Q

basal ganglia

A

central cholinergic neuron

striatal interneurons

antagonizes dopamine -> motor control

159
Q

brainstem pedunculopontine nucleus

A

central cholinergic neurons

REM sleep initiation

160
Q

dopamine nuclei

A

midbrain substantia nigra
midbrain ventral tegmental area
hypothalamus

161
Q

midbrain substantia nigra

A

dopamine nucleus

motor control via projection to basal ganglia

162
Q

midbrain ventral tegmental area

A

dopamine nucleus

mesolimbic/mesocortical tract –> motivation/activation/pleasure/reward/addiction

163
Q

hypothalamus

A

dopamine nucleus

tuberoinfundibular system releases DA to inhibit pituitary prolactin secretion

164
Q

nucleus acumbens

A

location of pleasurable/reward effect of dopamine (in forebrain)

165
Q

norepinephrine nuclei

A

locus ceruleus

166
Q

locus ceruleus

A

main NE nucleus related to behavior - wide projections to all cortical regions, cerebellum, spinal cord

implicated in:
arousal/awakening
increases attention
stress-mediated activation
ADHD, PTSD
mood and affect
pain modulation
167
Q

serotonin nuclei

A

raphe nuclei

168
Q

raphe nuclei

A

all levels of brainstem - pathways target all cerebral cortex

implicated in:
arousal, awakening, food intake
mood and affect
pain modulation

169
Q

dopamine, NE, serotonin

A

metabotropic receptors (except 5HT)

action terminated by reuptake transporters

transmitter release modulated by autoreceptors

excess transmitter metabolized by monoamine oxidase (MAO)

dopamine and NE also metabolized by COMT

170
Q

autoreceptors

A

receptors for a particular NT on presynaptic membrane

provide feedback: when too much NT in synapse, activation of autoreceptors decreases release of more NT

171
Q

depression risk factors

A 
genetics
stress
emotional trauma
comorbidities
post-partum
SAD
172
Q

Major Depressive Disorder

A

MDD

a least 5 of the following symptoms during same 2-week period:
depressed/irritable*
diminished interest*
weight loss/appetite disturbance
sleep disturbance
psychomotor agitation/retardation
fatigue
worthlessness
trouble concentrating
thoughts of death/suicide

*symptoms must be one of these

173
Q

anxiety risk factors

A 
genetics
emotional trauma
injuries, illness
loss/grief
stimulants
certain illnesses (hyperthyroidism)
infection
174
Q

anxiety disorders definition

A

caused by interaction of biopsychosocial factors interacting with situations, stress, trauma

symptoms vary

3 groups

175
Q

3 groups of anxiety disorders

A

anxiety
obsessive-compulsive
trauma/stressor-related

176
Q

anxiety disorders

A

panic
generalized
social
agoraphobia

177
Q

obsessive-compulsive/related disorders

A

OCD
body dysmorphia
hoarding

178
Q

trauma/stressor-related disorders

A

PTSD
acute stress
adjustment disorder

179
Q

regions of brain associated with depression

A

amygdala
prefrontal cortex
hippocampus
thalamus

180
Q

amygdala

A

limbic system

controls autonomic responses of fear, arousal, stress, formation of memories of emotional events

activated with emotionally-charged memory recall

changes in volume/activity observed in depression

increased activity observed to continue even when depression is resolved/remission

181
Q

prefrontal cortex

A

executive fxn of brain: discrimination btwn conflicting thoughts, planning complex cognitive behaviors, working toward a goal

inhibits activity of amygdala to allow focus on tasks

decreased PFC activity in depressed people (less suppression of amygdala)

182
Q

hippocampus

A

spatial orientation and long-term memory

depressed patients may exhibit memory loss or memory recall difficulties
-perhaps due to decrease in physical volume as well as fxn

183
Q

thalamus

A

receives sensory info and relays to cerebral cortex

links sensory input to pleasant/unpleasant feelings

arousal, wakefulness, alertness

increased size in part involved in emotion (increased # of neurons too)

184
Q

amine hypothesis of depression

A

increased synaptic amines produce secondary, downstream neuroplastic changes

involve transcriptional/translational changes in receptors and how they respond to 5HT and NE

b/c mood-elevating properties require weeks of treatment, despite immediate increases in amine NT transmission

185
Q

neurotrophic hypothesis of depression

A

increased stress hormones cause a decrease in brain-derived neurotrophic factor (BDNF) which causes hippocampal cell atrophy and reduce NT activity in hippocampus

antidepressants:

  • improve BDNF activity (promotes growth/survival of neurons in hippocampus)
  • promote growth factors in hippocampus (neurogenesis)
186
Q

other theories of depression

A

excess serum glucocorticoids cause hippocampus atrophy (more vulnerable b/c of many glucocorticoid receptors)

glutamate’s role (ketamine is a glutamate receptor antagonist)

disruptions in normal gut microbiota

SAD

187
Q

nonpharmacologic evidence-based approaches to depression

A 
counseling
electroconvulsive therapy
cognitive behavioral therapy
transcranial magnetic brain stimulation
vagal nerve stimulation
deep brain stimulation
phototherapy
exercise
188
Q

cognitive behavioral therapy in depression

A
  1. identify the thoughts and images that precede distressing emotions
  2. distance from beliefs that are embedded into these thoughts and images
  3. rationally question beliefs
  4. learn new behaviors and coping skills
189
Q

general clinical considerations for antidepressants

A

therapeutic lag
suicide risk
mania risk
adverse effects worst in first 1-2 wks

190
Q

serotonin syndrome

A

overstimulation of 5HT(IA) and possible 5HT(2) receptors

risk factors:
SSRI overdose
drug-drug interactions

symptoms:
altered mental status
autonomic instability
neuromuscular dysfxn
fever/hyperthermia
191
Q

SSRI MOA

A

inhibit reuptake of serotonin to increase concentration in synapse

192
Q

SNRI MOA

A

inhibit reuptake of serotonin and NE to increase concentrations in synapse

193
Q

MAO inhibitors

A

older class of antidepressants
2nd/3rd choice usually
as effective as TCAs/SSRIs, but more dangerous
hypertensive crisis risk w/ tyramine-rich diet
rigid diet required

194
Q

forms of MAOIs

A

MAO-A inactivates NE and 5HT
MAO-B inactivates DA

MAO-A metabolizes dietary tyramine in liver to inactive metabolites

all are nonspecific and will inhibit both types of MAO in brain

195
Q

MAOIs in brain

A

inhibit intraneuronal MAO-A to increase NE and 5HT available for release

increased transmission of NE/5HT

196
Q

tyramine and MAOIs

A

MAOIs increase NE in synapse

dietary tyramine not metabolized in gut - enters circulation

tyramine displaces NE into synapse - hypertensive crisis

197
Q

MOA of benzodiazepines

A

bind to site on GABA(a) receptor and potentiates GABA actions (no effect if GABA is not present)

at high doses barbiturates mimic GABA and are not limited by amount of GABA present

198
Q

excitable cells

A

ROM -70mV

when neuron depolarizes to threshold voltage, fast sodium channels open and neuron has an action potential

199
Q

steps of neuron firing

A
  1. graded depolarization brings trigger zone of axon hillock to threshold
  2. voltage-gated Na channels open –> rapid depolarization
  3. voltage-gated Na channels inactivated and voltage-gated K channels open –> repolarization
  4. slow inactivation of K gates –> hyperpolarization
  5. ion redistribution by Na/K pump restores RMP
200
Q

what depolarizes a cell to threshold?

A

chemical transmission (excitatory or inhibitory)

in healthy brain, balance between both so neurons don’t synchronously “fire” inappropriately

201
Q

summation

A

spatial
temporal

EPSPs and IPSP can cancel each other out

202
Q

good NT targets for seizures

A

glutamate

GABA

203
Q

good ion channel targets for seizures

A

sodium
calcium
chloride
potassium

204
Q

brain electrical activity while awake

A

widely distributed activity

205
Q

brain electrical activity while asleep

A

more synchronized - larger numbers firing in fewer places

206
Q

EEG

A

captures brain activity

207
Q

common causes of a single seizure

A 
head trauma
stroke
brain infection
tumors
eclampsia
hypoglycemia
drug/alcohol acute effect/withdrawal
childhood fever
208
Q

age-relatedi ncidence of epilepsy

A

u-shaped relationship

more common in older adults because of neurodegenerative diseases

GABA may have paradoxical (excitatory not inhibitory) effect on infants

209
Q

% of patients w/ uncontrolled seizures

A

1/3

b/c no available treatment works

210
Q

risk factors for developing epilepsy

A 
traumatic brain injury
brain tumor
stroke
CNS infections
dementia
hypoxia
Down Syndrome
Cerebral Palsy
autism
migraine w/ aura (esp. in children)
family Hx
febrile seizures past expected time frame
seizure in first mo. of life
recreational drugs
211
Q

seizure

A

single occurrence of S/Sx due to abnormal excessive or synchronous neuronal activity in brain

transient
paroxysmal

group of neurons abnormally hyperactive and hypersynchronous form an epileptogenic focus

disturbance of motor control, sensation, behavior, consciousness, autonomic fxn

212
Q

epileptogenic focus

A

area of brain from which seizure emanates

fxns autonomously, causing excessive paroxysmal electrical discharges

213
Q

prodrome

A

difficult to describe feeling that a seizure may occur - minutes to hours before

anecdotal evidence of “seizure alert dogs”

214
Q

aura

A

particular sensory. autonomic or psychic symptom at the beginning of a seizure that is characteristic of seizures

215
Q

ictal phase

A

period of time from first symptom (including aura) to end of seizure activity

216
Q

epilepsy syndromes

A

clustering of findings of seizures with other clinical phenomena define specific epilepsies

incidence may be unique to a given age group

in some cases a specific gene mutation is the cause

217
Q

epilepsy

A

any of the following:

  • 2 unprovoked/reflex seizures more than 24 hrs apart
  • 1 unprovoked/reflex seizure and probability of further seizures at least 60% after two unprovoked seizures, occurring over next 10 years
  • diagnosis of epilepsy syndrome
218
Q

resolution of epilepsy

A

person with age-dependent epilepsy syndrome but are past the applicable age or have been seizure-free for 10 years, with no seizure medicines for last 5 years

219
Q

broad types of seizures

A

focal and generalized

220
Q

focal seizures

A

also called partial

activity begins in one limited area of brain

221
Q

simple partial seizures

A

awareness, consciousness, memory preserved

may have focal motor, sensory, autonomic or psychic signs

222
Q

complex partial seizures

A

any impairment of awareness or consciousness

may display automatisms: repeating same word, picking at fabric, smacking lips, freezing completely (may have aura; common site is temporal lobe)

223
Q

second generalization

A

starts in one focal area, then spreads and becomes generalized

224
Q

generalized seizures

A

more severe

synchronous electrical activity throughout brain

225
Q

absence seizures

A

petit mal

stare w/ unresponsiveness, rapid recovery

mouth may move, eyes may blink. very brief

more common in children. can be mistaken for daydreaming.

226
Q

tonic/clonic seizures

A

grand mal

long lasting, unmistakable motor signs, may bite tongue, become incontinent, slow postictal recovery.

loss of consciousness

227
Q

tonic phase

A

stiffening of all muscles

person will cry out, groan, shriek as air is forced past vocal cords.

loses consciousness and falls down

long post-ictal phase of drowsiness, confusion, amnesia

228
Q

clonic phase

A

jerking phase

extremities jerk rhythmically and rapidly

229
Q

atonic seizure

A

drop seizure

sudden loss of muscle tone. person may drop to ground, drop what they are holding, etc.

230
Q

myoclonic seizure

A

brief muscle jerks

231
Q

status epilepticus

A

repeated seizures w/o pause. medical emergency

232
Q

clinical manifestations of seizures

A

changes in motor control, sensation, behavior, consciousness, autonomic fxn

in focal seizures: may provide clue to localization of epileptigenic focus

in generalized seizures: progression of signs/history can give hints regarding location

careful history needed (pre- and post-ictal characteristics)

233
Q

common comorbidities of seizures

A

psychiatric
cognitive
social

234
Q

frontal lobe seizure symptoms

A

disruptive behavior

running, screaming, fear, anger, aggression, swearing

235
Q

temporal lobe seizure symptoms

A

changes in sense of smell, odd odors, smell that isn’t there

OR

block speech, produce typical automatic movements, repetition

OR

alter consciousness/mood

OR

illusions of sounds

236
Q

occipital lobe seizure symptoms

A

visual distortions/images of things not there

237
Q

seizure triggers

A

vary from person to person

missed/skipped AED dose
sleep deprivation
fever, illness
flashing lights/bright patterns
alcohol/drug use/withdrawal
stress
menstrual cycle
hypoglycemia
poor dietary intake
specific foods, excess caffeine
medicatons that lower threshold
238
Q

catamenail epilepsy

A

increase in seizures during specific times of the menstrual cycle

239
Q

organ dysfxn in seizures

A

neurons organized in circuits with synaptic links btwn thalamus and cortex

w/in cortex, wave of excitation often followed by inhibition, due to inhibitory neurons using GABA

if sufficient neurons fire together/are inhibited/fire again, synchronized depolarization/hyperpolarization can be detected on EEG as large waves

focal seizure may only show up on a few leads

generalized seizure has more widespread activity

worse case scenario: severe, treatment-refractory, status epilepticus and brain death

240
Q

general mechanisms of seizures and epilepsy

A

disruption in balance between neuronal excitation and inhibition

too much excitation or
too little inhibition

241
Q

sources of neuronal excitation

A

brain: abrupt source of sensory input

cell: opening channels permeable to Na and Ca
- activation of receptors for glutamate

242
Q

sources of neuronal inhibition

A

brain: sleep

cell: opening K or Cl channels
- increased GABA or increased activity of GABA receptors

243
Q

nonpharmacologic epilepsy treatments

A

ketogenic diet
vagal nerve stimulation
surgery

244
Q

therapeutic goals for controlling seizures

A

early control to allow maintenance of as normal a life as possible

decrease frequency and severity

prevent recurrence

245
Q

effects of antiepileptic drugs

A

raise seizure threshold by stabilizing neuronal membranes and suppressing discharge of neurons

suppress propagation of seizure activity by reducing nerve conduction and synaptic transmission

246
Q

mechanisms of action for antiepileptic drugs

A

suppress sodium influx
suppress calcium influx
glutamate antagonism
GABA potentiation

247
Q

seizure treatment algorithm

A
  1. start with one AED
  2. trial alternative agent (cross-taper)
  3. consider AED combo treatment
248
Q

drug evaluation for AEDs

A

trial period
dosage adjustment
seizure frequency chart

249
Q

plasma drug level monitoring for AEDs

A

monitors adherence
determines cause of lost seizure control
identifies toxicity causes

adjusting initial doses increass potential for rapid seizure control

most important for major convulsive seizures

250
Q

patient nonadherence in seizures

A

50% of treatment failures

promote adherence:

  • education about chronicity of epilepsy
  • monitor plasma levels
  • seizure frequency chart

taper 6 wks to several months

251
Q

suicide risk with AEDs

A

FDA blanket warning, esp. topiramate and lamotrigine

carbamazepine and valproic acid may be protective

not assoc. w/ AEDs
more due to illness
suicide/attempts very rare b/c of AEDs

screen all patients for comorbid depression/anxiety

252
Q

managing status epilepticus

A

maintain ventilation
correct hypoglycemia
terminate seizures w/ drugs
initiate/start long-term rugs

Pathophysiology, Pharmacology, and Therapeutics (7 decks)

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