Clinical Reasoning + Endocrine Hormones Review Flashcards
1
Q
premature closure
A
concluding evidence gathering and making a diagnosis prior to thorough reflection on all data. commonly associated with pattern recognition
2
Q
false consensus
A
form of premature closure. offer limited analysis/information because you believe that others have reached an identical conclusion
3
Q
confirmatory bias
A
tendency to seek or favor data that confirms one’s preferred diagnosis while ignoring or disregarding data that would disfavor the diagnosis
4
Q
unintentional sequestration of data
A
pertinent information is unintentionally omitted by someone on the team; eg clinical sign, previous medical history, etc
4
Q
illusory transactive memory system
A
related to unintentional sequestration of data- provides medical team with a deceptive sense of security that because you’re working with a team, someone before you got all the data that you need. “someone must’ve read the chart”
4
Q
contagious illusion
A
respect for authority or desire for consensus allows data to be interpreted as valid by others; eg a supervising clinician states that a collection of clinical signs means the patient has _____ disease
4
Q
what medical error can be summarized to “someone must have read the chart”?
A
illusive transactive memory system
5
Q
selective perception
A
expectations influence your senses such that you can feel, hear or see something that you expect to hear
6
Q
recency effect
A
the most recent events in the patient’s medical history or disease are more heavily weighted than the events that occurred earlier
6
Q
what medical error can be summarized in “well the patient seems like it has heart disease, so I should be hearing a heart murmur”
A
selective perception
7
Q
primacy effect
A
initial events in the patient’s medical history or disease are weighted more heavily than events that occur later
8
Q
what are the 4 clinical reasoning strategies?
A
- pattern recognition
- arborization
- exhaustive search
- hypothetical-deductive method
8
Q
availability heuristic
A
estimating what is more likely by what is most available in your memory: biased towards vivid, unusual, or emotionally charged examples
9
Q
what are the pros and cons of pattern recognition?
A
pros: quick/efficient, cost-effective, common things look common, quick treatment, life saving!
cons: misdiagnosis, wrong treatment, experience matters, location matters, can lead to rush to judgement, increased morbidity/mortality
10
Q
what are pros and cons of arborization?
A
pros: unusual differentials, need a pathway to lead to one or other, emergent situations or referrals
cons: doesn’t account for comorbidities, only as good as their designer
11
Q
what are pros and cons of exhaustive search?
A
pros: rare disease!
cons: overwhelming, often go to as last resort, time consuming, unnecessary diagnoses
12
Q
what are pros and cons of the hypothetical-deductive method?
A
pros: orderly, kinda ties things together
cons: slow, experience matters
12
Q
what are the best reasoning strategies?
A
all are used, but best are pattern recognition and hypothetical-deducation
12
Q
why is the clinical reasoning cycle important?
A
reminds you to be systematic in your approach to cases
self-awareness/metacognition is part of expert reasoning!
13
Q
what strategy is our model based on?
A
hypothetical-deductive strategy
13
Q
what clinical reasoning strategy can be summarized as
“it just looks like a case of…”
A
pattern recognition
14
Q
what clinical reasoning strategy is summarized as “if this is true, then do this…”
A
arborization (decision trees)
15
Q
what clinical reasoning strategy is basically the bread and butter of vet school?
A
exhaustive search: gather, then sift
16
Q
why do we care about clinical reasoning strategies?
A
mistakes happen! need to be aware of what you did to lead your decisions. was it a strategy error? a cognitive error? systemic problem?
17
what are the steps in the clinical reasoning cycle?
1. identify patient
2. acquire data
3. summarize data
4. list problems
5. generate differentials
6. justify differentials
7. identify top differentials
8. acquire data
17
how do you organize a case summary (history and PE)
1. signalment and chief complaint
2. history of current problem
3. background history
4. physical exam
18
what does the liver store glucose as?
glycogen
19
what cells release glucagon?
alpha cells of pancreas release glucagon into blood
20
what breaks down glycogen to release glucose into blood?
liver
21
is insulin anabolic or catabolic?
anabolic
increases storage of glucose, fatty acids and amino acids
22
is glucagon anabolic or catabolic?
catabolic
increases mobilization of glucose, fatty acids, and amino acids
23
what does insulin do to energy production?
suppresses it: allows cellular uptake of glucose
suppresses fat lipolysis, fatty acid oxidation, gluconeogenesis, glycogenolysis
24
without insulin, what happens to the body?
hyperglycemia, hyperlipidemia, ketones
no glucose uptake, fatty acid oxidation occurs (ketones), fat lipolysis occurs, gluconeogenesis occurs
25
history and PE of DM
weight loss with polyphagia
PU/PD
cataracts (dogs only)
recurrent infections (UTIs)
hepatomegaly
26
what species gets cataracts with DM?
dogs only
26
with a dog with weight loss, what do you ask about first?
appetite!
27
what are 3 causes for polyphagia
1. inadequate intake
2. hypermetabolism
3. nutrient loss
28
what are the 4 causes of anorexia
1. primary anorexia
2. pseudoanorexia
3. primary GI
4. secondary GI
29
what causes PU/PD?
osmotic diuresis: glucose is an osmotic agent. water channels are in tubules and water leaves due to the gradient. osmolality of urine is increased
30
what causes cataracts in dogs with DM?
normally, glucose is processed thru anaerobic glycolyic pathway and turned into lactic acid, which readily diffuses out of lens normally
when glucose overwhelms the cells, it goes thru the sorbitol pathway and becomes sorbitol + fructose. it then can't diffuse out and water builds up in the lens
31
clinicopathologic changes of DM
- hyperglycemia
- glucosuria
- elevated cholesterol
- elevated liver enzymes
- minimally concentrated urine
32
renal thresholds of glucose
dogs: 180 mg/dL
cats: 250 mg/dL
once threshold exceeded, you get spillover into urine and thus glucosuria
33
why do you see elevated cholesterol with DM?
lack of insulin = fat metabolism derangement
lipoprotein lipase = impaired: normally clears VLDLs and triglycerides
LDL receptor impaired: clears cholesterol
33
what are the important mineralocorticoids produced in the adrenal glands?
aldosterone, RAAS
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what are the important glucocorticoids produced in the adrenal glands?
cortisol, ACTH
35
where are the mineralocorticoids produced?
glomerulosa
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where are the glucocorticoids produced?
fasciculata
37
what determines production of aldosterone and cortisol?
enzymes
aldosterone: aldosterone-synthase
cortisol: 17-a-hydroxylase
38
what is the 1st step in steroid synthesis?
endogenous ACTH stimulation initiates the first step. binding induces cascade of cortisol
38
what is the axis of stress?
hypothalamic-pituitary-adrenal-axis
39
describe the pathway of the HPAA
1. hypothalamus produces CRH
2. CRH stimulates the pituitary to produce ACTH
3. ACTH stimulates the adrenal glands to make cortisol
negative feedback stops this
40
what produces CRH?
hypothalamus
41
what produces ACTH?
pituitary
42
describe the consequences of a pituitary tumor
pituitary-dependent hyperadrenocorticism
both adrenal glands become hyperplastic. produce tons of cortisol, but there is no suppression to pituitary because the tumor just does its own thing
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describe the consequences of an adrenal tumor
one adrenal gland produces TONS of cortisol, which gives lots of feedback to pituitary telling it to turn off. you get pituitary atrophy.
then get contralateral adrenal gland atrophy due to lack of stimulation
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describe consequences of iatrogenic cushing's
suppression of pituitary (ACTH) by exogenous steroids
only the fasciculata atrophy. both adrenal glands atrophy because the pituitary is not stimulating them
47
typical addison's
immune-mediated destruction of BOTH zona fasciculata and zona glomerulosa. thus cortisol AND mineralocorticoids are low
48
in typical addison's, what is low?
cortisol and mineralocorticoids
48
atypical addison's
immune-mediated destruction of ONLY zona fasciculata
only cortisol low
49
in atypical addison's, what is low?
only cortisol is low
50
metabolic effects of cortisol
- floods the body with energy: proteins/glucose/fat to deal with stress
- maintains blood pressure
- dampens inflammatory cascade
50
how does cortisol affect energy recruitment?
- increases glucose for energy: gluconeogenesis
- breaks down protein to feed gluconeogenesis
- liberates lipids for beta oxidation
51
is cortisol anabolic or catabolic?
catabolic! breaks down glycogen, fat, etc. muscle wasting of apaxial muscles typical, get pot belly and redistribution of fat to abdomen and nape of neck
(opposite is hot abs from testosterone)
52
vascular effects of cortisol
- helps maintain vascular response to hypovolemia
- permissive effect in conjugation with catecholamines
53
what is the vascular effect of a cortisol deficiency?
hypotension
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what is the vascular effect of a cortisol excess?
hypertension
54
anti-inflammatory effects of cortisol
- inhibits phospholipase A2
- prevents formation of important inflammatory products
- cortisol excess leads to immunosuppression: pyoderma, UTI, etc
55
where are common locations of endocrine alopecia?
lateral thorax and abdomen, perineum and caudal thighs
head, neck and extremities spared
55
CNS effects of cortisol
polyphagia, polydipsia
cortisol excess and deficiency both cause PU/PD!! but by different mechanisms
56
what is cortisol's effect on the GI system?
maintenance of the GI mucose
cortisol deficiency leads to vomiting and bloody diarrhea
56
what are cortisol's effects on CBC?
- RBC production, suppresses lymphocytes and eosinophils
- prevents migration of neutrophils out of circulation
- see neutrophilia but immunosuppression because the neutrophils can't get to the site of infection!
57
what CBC abnormalites will you see with a cortisol excess disorder?
stress leukogram
58
what CBC abnormalities will you see with cortisol deficiency?
lack of stress leukogram and anemia
59
biochemistry abnormalities with a cortisol excess
- increased ALP/GST: steroid-induced isoenzyme and excessive glycogen
- increased cholesterol: increased lipolysis
- increased glucose (mild): increased gluconeogenesis
60
biochemistry abnormalities seen with a cortisol deficiency
- increased ALT: shock
- decreased cholesterol: decreased GI uptake
- decreased glucose: decreased gluconeogenesis
- increased K+ and decreased Na : decreased mineralocorticoids
61
urinalysis abnormalities seen with excess cortisol
- decreased USG: ADH inhibition?
- proteinuria: multifactorial
- bacteriuria without pyuria: immunosuppression (no evidence of WBC because neutrophils are stuck
62
urinalysis abnormalities seen with a cortisol deficiency
decreased USG: decreased mineralocorticoids
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thyroid hormone ingredients
- iodide trapping mechanism
- thyroglobulin
- tyrosine
- iodine
- thyroid peroxidase
64
what is thyroglobulin?
a protein that creates the string that tyrosine attaches onto
65
what are the steps of making thyroid hormone?
organification and synthesis
66
how is thyroid hormone secreted and transported?
- poorly water soluble; uses thyroxine-binding globulin (TBG) to get into cell
- nearly all >99% of T4/T3 is bound to proteins
- inactive when bound
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when is thyroid hormone inactive?
when it is bound - nearly all of T4/T3 is bound to proteins
68
thyroid hormone action at the cellular level
- delivered to receptors in the nucleus
- forms a hormone-receptor complex
- result: gene transcription or inhibition
69
what is the result of thyroid hormone forming a hormone-receptor complex at the nucleus?
gene transcription or inhibition
70
what is the thyroid axis?
1. hypothalamus: TRH: thyrotropin releasing hormone
2. pituitary gland (anterior): thyroid stimulating hormone (TSH)
3. thyroid gland: T4 and T3
71
how can thyroid affect growth?
disproportionate dwarf: lack of thyroid hormone
proportionate dwarf: lack of growth hormone
72
what are the thyroid effects?
growth, development, metabolism, specific systems
73
what is the difference between a disproportionate dwarf and a proportionate dwarf?
disproportionate dwarf is a lack of thyroid hormone
proportionate dwarf is a lack of growth hormone
74
how does thyroid hormone affect development?
mammals: fetal and neonatal brain development
reptile: metamorphosis won't occur if frog is deficient in thyroid hormone
75
how does thyroid hormone affect metabolism?
increases basal metabolic rate
- stimulates lipolysis
- increases carbohydrate uptake from the gut
- increases gluconeogenesis and glycogenesis
- increases insulin-dependent glucose uptake into cells
- protein catabolism: energy recruitment
76
what cardiovascular effects are seen with a hypothyroid dog?
none; rarely clinically significant
76
what cardiovascular effects can be seen with a hyperthyroid cat?
hyperthyroidism upregulates the number and affinity of beta-adrenergic receptors
increases cardiac output, leading to tachycardia, +/- arrhythmias, murmurs
hypertension
77
what CNS effects are seen with a hyperthyroid cat?
upregulates adrenergic activity? nervousness, hyperactivity, aggression
78
what CNS effects are seen with a hypothyroid dog?
mental dullness
79
what PNS effects are seen with a hyperthyroid cat?
little clinical significance
80
what PNS effects are seen with a hypothyroid dog?
- demyelination and decreased action potential
decreased reflexes, forelimb/hindlimb paresis, cranial nerve deficits
81
what skin effects are seen in a hyperthyroid cat?
unkempt haircoat
82
what skin effects are seen in a hypothyroid dog? what is the mechanism?
hair gets "stuck" in telogen (resting) stage. alopecia in areas of wear, lack of regrowth after clipping, hyperpigmentation
83
what other organs are affected by abnormal thyroid levels?
excess thyroid: looking for energy, extra O2 consumption, increased cardiac output, increased renal blood flow. get muscle wasting, fat loss, tachypnea, PU/PD
deficiency in thyroid: weight gain
84
how does thyroid hormone affect CBC?
excess: increased O2 consumption in bone marrow, rarely increased PCV
clinically insignificant in both counts
85
what abnormalities are seen on a biochemistry panel of a hyperthyroid cat?
liver hypoxia from increased O2 consumption?
- increased gluconeogenesis and protein breakdown leads to increased liver enzymes (ALT > ALP), increased BUN, mild increase in glucose
86
what biochemistry panel abnormalities might you see with a hypothyroid dog?
disrupted cholesterol synthesis and degradation: increased cholesterol
87
what abnormalities would you see on a urinalysis of a hyperthyoid patient?
increased CO --> increased renal blood flow --> medullary washout: losing fluid
see decreased USG
88
is the parathyroid gland stimulated by increased or decreased calcium?
decreased calcium
parathyroid hormone from chief cells
PTH props it up!
89
what abnormalities would you see on a urinalysis of a hypothyoid patient?
none
90
is the thyroid gland stimulated by increased or decreased calcium?
increased calcium
calcitonin from C cells (parafollicular cells)
calci-tone-in tones it down!
91
how does calcium maintain homeostasis?
45-50% protein bound, same amount is ionized (active). 5-10% is complexed with other molecules like phosphate, citrate, bicarb
92
what is the mass law effect?
total calcium x total phosphorus = <60
don't want to exceed 60: will see mineralization of tissues
93
the parathyroid gland gets activated by decreased calcium levels. what does it signal in attempts to raise these?
- bone: increases bone resorption
- kidneys: increases Ca2+ reabsorption, which increases P excretion, thus decreasing levels of Phosphorus
- kidneys start producing more vitamin D: which pulls Ca and P in from the GI tract
94
what does vitamin D do in calcium regulation?
Vitamin D is produced by the kidneys, it pulls Ca2+ and Phosphorus in from the GI tract
95
what effect does PTH have on Ca2+ and PO4?
Ca2+: increases levels
PO4: decreases levels
mass law
96
what effect does calcitonin have on Ca2+ and PO4?
decreases both
97
what effect does vitamin D have on Ca2+ and PO4?
increases both
98
what are the hypercalcemia rule-outs?
GOSHDARNIT
G: granulomatous: fungal
O: osteolytic
S: spurious
H: hyperparathyroidism
D: vitamin D toxicosis
A: addison's disease
R: renal secondary hyperparathyroidism
N: neoplasia
I: idiopathic
T: toxins
99
granulomatous causes of hypercalcemia
- fungal: blastomycosis and others
- bone invasion?
- abnormal vitamin D metabolism by macrophages?
100
osteolytic causes of hypercalcemia
osteolytic = tumor
- osteoClast activating factors
- Calcium
- osteosarComa
101
spurious causes of hypercalcemia
not real or not abnormal; not pathologic
- lipemia
- hemolysis from sample handling
- hemoconcentration
- hyperalbuminemia : doesn't actually change iCa2+
- acidosis: favors dissociation of Ca2+ from proteins
- young animal
102
hyperparathyroidism and hypercalcemia
- excessive production of PTH
- parathyroid adenomas
- parathyroid hyperplasia
103
vitamin D toxicosis cause of hypercalcemia
- rodenticides: cholecalciferol
- treatments for psoriasis
- over supplementation
104
addison's disease and hypercalcemia
usually mild total calcium elevation: iCa2+ usually normal
105
renal secondary hyperparathyroidism and hypercalcemia
- decreased vitamin D production from kidneys
- phosphorus retention from kidney dysfunction
106
in renal secondary hyperparathyroidism, the kidneys are not functioning properly. they have decreased excretion of phosphorus, which in turn has what effect on calcium? why?
decreased excretion of phosphorus means there is increased serum phosphorus, and because of the mass law effect, this increase causes a decrease in serum Ca2+. this will tell the parathyroid gland to increase PTH levels
107
neoplasia and hyperparathyroidism
PTH-related proteins: PTHrp: protein that parathyroid gland reads and shuts off. PTHrps take over and increase Ca2+
107
why do you need to be careful with what types of calcium you are measuring?
in renal secondary hyperparathyroidism, total calcium is often elevated, but ionized calcium is often normal or decreased. this is what is driving the overproduction of PTH
108
what are the most common tumors causing hypercalcemia?
LYMPHOMAAA
apocrine gland adenocarcinomas of the anal sac: AGASACA
109
what species is known for idiopathic hypercalcemia?
cats
110
what toxins lead to hypercalcemia?
- plants: day blooming jessamine
- vitamin D
111
what are clinical signs of hypercalcemia? why?
- PU/PD
- weakness, listlessness
- inappetance
- cardiac arrhythmias
- calcium oxalate stones
- UTIs?
many of these due to decreases in depolarization
112
what are clinical signs of hypocalcemia?
- muscle fasciculation/tetany
- pruritus/facial rubbing
- panting
- nervousness
- seizures
- cardiac arrhythmias
many of these due to rapid depolarization
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