Endocrine/Neuro Flashcards
(114 cards)
1
Q
this system regulates growth maturation, metabolic function, fluid balance, responses to stress, and reproduction through the action of the hormones they secrete
A
endocrine system
2
Q
endocrine disorder that is an intrinsic malfunction of the hormone-producing gland
A
primary
3
Q
endocrine disorder that results from an abnormal pituitary secretion of trophic hormones signals (main problem)
A
secondary
4
Q
feedback loop Figure 20-2B!!!!
A
Study It!!
5
Q
type of thyroid disorder in which the thyroid glad itself fails:
o inadequate hormone produced by the thyroid
–> low levels of circulating hormone
o blood levels of the corresponding trophic pituitary hormone are very elevated
A
Primary
6
Q
type of thyroid disorder in which the pituitary gland fails:
o release of the trophic hormone is significantly decreased –> Secondarily reducing primary gland function so both levels are abnormally low thyroid hormones
A
Secondary
7
Q
T3 and T4 are regulated by the ______ ______ ______ that is secreted from the anterior pituitary
A
thyroid stimulating hormone (TSH)
8
Q
thyroid stimulating hormone (TSH) is secreted from the _________
A
anterior pituitary
9
Q
Thyroid hormones produced in the follicular cells of the thyroid that regulate metabolism, required for growth and development of tissue
A
o T3 – triiodothyronine
o T4 – thyroxine
10
Q
“Thyrotoxicosis”– condition that results from any cause of increased TH levels
A
hyperthyroidism
11
Q
Types of _________:
o Hashimotos- first stages of Hashimotos when there is a release of T3 and T4 d/t thyroid cell destruction (hyperthyroidism)
o Toxic multi nodular goiter
o Solitary toxic adenoma
A
Hyperthyroidism
12
Q
the most common cause of hyperthyroidism that is a result of stimulation of thyroid cells with autoantibodies against TSH receptor (Type II hypersensitivity where the target cells of the thyroid are not destroyed but malfunction)
A
Grave’s Disease
13
Q
Patho of _______:
Auto-antibodies bind and activate with receptors for TSH and stimulate production of T4
As the T4 rises in the system, the pituitary decreases the production of TSH
The etiology is autoimmune (Grave’s Disease genetic markers)
Feedback loop out of commission
A
Grave’s Disease
14
Q
Clinical Manifestations of \_\_\_\_\_\_\_: >Adrenergic stimulation – d/t increase in T4 tachycardia nervousness lid lag (associated w/ exophthalmos) tremor increased B/P >Excess T4 increased O2 consumption changes in protein metabolism increase in metabolic rate decrease in weight heat intolerance inability to concentrate amenorrhea in women (scant menses) >Immunologic stimulation – goiter
A
Grave’s Disease
15
Q
Triad of Symptoms of Grave’s Disease
A
o Hyperthyroidism
o Exophthalmos
o Goiter
16
Q
very high levels of T4 that is life-threatening resulting in increased temperature, severe tachycardia, arrhythmias, congestive heart failure, extreme restlessness, psychosis
***may be triggered via stress or gland manipulation in people who have hyperthyroidism
A
Thyroid Storm
17
Q
type of hypothyroidism that accounts for the majority of cases d/t the intrinsic thyroid gland dysfunction that results from:
o Congenital, defective hormone synthesis, iodine deficiency, anti-thyroid drugs, iatrogenic loss of thyroid tissue
o Congenital aka critinism d/t thyroid dysgenesis or lack of development of thyroid gland
A
Primary
18
Q
type of hypothyroidism that is related to pituitary or hypothalamic failure (usually r/t head or brain conditions) caused by pituitary tumor or treatment of tumor
A
Secondary
19
Q
Labs for Diagnosis of ______:
o Low T4 (b/c thyroid is not producing it the way it should)
o High TSH (b/c the anterior pituitary is trying to get the thyroid to produce more T4)
A
Hypothyroidism
20
Q
Causes of _______:
o Acute and subacute thyroiditis
o painless thyroiditis
o postpartum thyroiditis
A
Primary Hypothyroidism
21
Q
with a patho similar to Hashimoto, this generally occurs 6-12 months postpartum with spontaneous recovery in most cases
A
postpartum thyroiditis
22
Q
Most common cause of acquired hypothyroidism caused by gradual inflammatory destruction of thyroid tissue by circulating auto-antibodies and infiltration by lymphocytes
A
Hashimoto’s (Lymphocytic Thyroiditis or Autoimmune Thyroiditis)
23
Q
Diagnosis of ______:
presence of thyroperoxidase and thyroglobulin antibodies
A
Hashimoto’s
24
Q
lack of iodine results in lack of ___ and ___
A
T3 and T4
25
lack of T3 and T4 stimulates TSH secretion which causes the thyroid cells to secrete large amounts of thyroid globulin which leads to ______
goiter
26
type of hypothyroidism caused by radiation of the thyroid gland or when they surgically remove the thyroid gland
iatrogenic
27
Lab Diagnosis of ______:
Decreased T3 & T4 which leads to...
Increased TSH
****Sensitive test we have for TSH is going to start detecting elevation levels of TSH before we have a significant amount of drop in the T3 and T4 & is used as a screening device and a monitoring device.
Hypothyroidism
28
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Clinical Manifestations of _______ in ______:
dull appearance
thick-protruding tongue
thick lips
prolonged jaundice
poor muscle tone
umbilical hernias are common
bradycardia with a hoarse cry
mental retardation if not treated
```
Hypothyroidism in Newborns
29
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Clinical Manifestations of _______ in _______ and ______:
decrease metabolic rate
weakness
lethargy
cold intolerance
decrease appetite
bradycardia
moderate weight gain
elevated serum cholesterol and triglycerides
enlarged thyroid
dry skin
constipation
depression
loss of lateral portion of eyebrow
women- irregular menses
```
Hypothyroidism in Children and Adults
30
generalized non-pitting edema, decreased level of consciousness, hypotension, hypothermia that occurs in severe or prolonged hypothyroidism and may progress into coma
myxedema
31
system that provides precise monitoring and control of the cellular environment which is important for maintaining hormone levels within physiologic ranges
feedback systems
32
Most common type of feedback that occurs when a changing chemical, neural, or endocrine response decreases the subsequent synthesis & secretion of a hormone
Regulation is possible at 3 levels
Negative Feedback
33
Possible Regulation Levels of _______:
• Target organ (ultra-short feedback)
• Anterior pituitary (short feedback)
• Hypothalamus (long feedback)
Negative Feedback
34
Type of feedback that occurs when a chemical, neural, or endocrine response increases the synthesis and secretion of a hormone or when an increased hormone level further increases the synthesis and secretion of that same hormone
Positive Feedback
35
TH is regulated through a ______ feedback loop
negative
36
TH negative feedback loop involves the ______ (3)
hypothalamus
anterior pituitary
thyroid gland
37
TH negative feedback loop is initiated by _______
TRH (thyrotropin-releasing hormone)
38
________ is synthesized and stored in the hypothalamus
TRH (thyrotropin-releasing hormone)
39
TRH (thyrotropin-releasing hormone) levels increase with exposure to ______ or ______ and from decreased levels of _____
cold or stress/ T4
40
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Regulation of __________:
TRH is released into the hypothalamic-pituitary portal system
-->Circulates to the anterior pituitary
-->stimulates release of TSH
-->causes release of stored TH
-->increase in TH synthesis
```
Thyroid Hormone Secretion
41
As levels of TH rise, there is a negative feedback effect on the HPA that inhibits release of _____ and ____
-->results in decreased TH synthesis and secretion
TRH and TSH
42
DM caused by absolute insulin deficiency caused by the destruction of the beta cells of the Islet of Langerhans of the pancreas
DM Type I
43
DM caused by insulin resistance in peripheral tissue so there is a deficient amount of insulin secreted from the pancreas
DM Type II
44
insulin helps glucose enter into the _____(3)
liver (glycogen)
muscles (energy)
adipose tissue (fat)
45
Glucose is supplied to the blood stream from the ____ and _____
GI track and the liver
46
Glucose is more abundant in ______ than in _____
extracellular fluid than inside cells
47
major glucose transporter for the blood brain barrier that is insulin independent (they can be transported across the cell membrane for a specific tissue without insulin)
Glut 1
48
glucose transporter in the liver and in a small part in the pancreatic beta cells that is insulin independent (they can be transported across the cell membrane for a specific tissue without insulin)
Glut 2
49
glucose transporter needed for glucose to be used by the neurons that is insulin independent
Glut 3
50
the only Insulin DEPENDENT glucose transporter found in muscle and adipose tissue
Glut 4
51
If there is no insuline, Glut 4 is sequestered in the _______
vesicles of the cells
52
In the presence of insulin, Glut 4 will move to the ______ to allow glucose to enter into the cell
plasma membrane
53
Type I DM affects more _____
males
54
Type I DM risk marker chromosome
human leukocyte antigen gene on chromosome 6
55
Congenital Nature of _____:
virus or other environmental insult occurs
-->insulin auto-antibodies and glutamic acid decarboxylase are produced
-->damage to the islet cells
-->Hyperglycemia
DM Type I
56
total absence of insulin and excessive glucagon d/t an increase in glucose that does not shut down the production of glucagon in the liver
Hyperglycemia
57
Patho of ______:
There is a genetic predisposition and environmental factors that combine to produce autoantigens that form on the insulin producing beta cells and circulate in the blood stream. This leads to a processing and presentation of autoantigen by Antigen Presenting Cells (APC’s) and the activation of the T-Helper 1 and T-Helper 2 lymphocytes
***Fig 21-13***
DM Type I
58
stage of beta cell destruction in Type I DM of Macrophage Activation in which lymphocyte and macrophage infiltration of the islets results in inflammation (insulinitis) and islet beta-cell death
Stage A
59
stage of beta cell destruction in Type I DM of Autoantigen Specific T Cytotoxic Cells Activation that consists of production of autoantibodies against islet cells, insulin, glutamic acid decarboxylase (GAD), and other cytoplasmic proteins
Stage B
60
Activation of B-Lymphocytes to produce Islet cell autoantibodies and destruction of the beta cells then follows with corresponding decrease in insulin secretion
Relative inactivity of T reg cells that contribute to a decrease in beta-cell mass and insulin production
Stage C
61
At Risk Ethnicities for _____:
Native Americans (Southwestern- Pima Indians)
Hispanics
Blacks
DM Type II
62
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Risk Factors for ______:
Age >40
Obesity (most powerful risk factor)
family history
member ethnic minority
female
```
Type II DM
63
Patho of _____:
o Genes influence insulin resistance (60-80% of cases of DMII) or beta cell dysfunction with the underproduction of insulin OR both
o May also see abnormal glucagon secretion (important in relation to prescribing pharm)
o Beta cell function (or dysfunction) is affected due to amyloid deposits (fatty deposits in pancreas and liver) or pancreatic fibrosis or cytokine toxicity
insulin is still produced for a time but eventually there will be complete destruction and the insulin will be completely gone
DM Type II
64
In ______, glucose enters the blood stream and the pancreas produces insulin, but it may not be enough to overcome the peripheral insulin resistance. This glucose is unable to enter the body cells effectively and glucose levels increase in the blood stream.
Type II DM
65
the fetal siphon needs ___ mg/kg every minute per kg of the fetal weight for every minute during gestation
6
66
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Risk Factors for _____:
family history (esp 1st degree relative)
ethnic group
age >25 years old
prior history of GDM or PCOS
overweight
Hx of OB complication
Hx of large baby greater 4000g
miscarriage 2-3 times
having a baby with a congenital anomaly
```
Type II DM
67
Insulin deficiency and an increase in the insulin counterregulatory hormones (i.e., catecholamines, cortisol, glucagon, and growth hormone
Ketoacidosis
68
In ketoacidosis,
Hepatic glucose production ______ and
peripheral glucose usage _______
increases
| decreases
69
In ketoacidosis, _________ decreases the pH (acidic) of the blood, creating a metabolic acidosis
ketogenesis (breakdown of ketones)
70
compensation for metabolic acidosis in ketoacidosis is________
Kussmaul respirations (trying to blow of acid)
71
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DM Type 2 complication that occurs more often in elderly patients (in particular---elderly pts with comorbidities) in which there is an increase in glucose, increase in serum osmotic pressures that leads to:
• severe dehydration
• low blood volume
• low perfusion pressure
death if it is not corrected
```
Hyperosmolar Hyperglycemic Non-Ketotic Syndrome (HHNK Syndrome)
72
Hypoglycemia followed by a rebound hyperglycemia that occurs d/t the counter-regulatory hormones that are stimulated by the hypoglycemia (glucagon, epinephrine/adrenaline, cortisol, and growth hormone)
**usually triggered (the up and down effect) by an excessive carbohydrate intake that starts the up-and-down
Somogyi Effect
73
recurrent or persistent hyperglycemia that will cause glucose binding to the red blood cells (RBCs)
Non-enzymatic glycosylation
74
what we are measuring when we measure Hgb A1C
Glycosylated Hemoglobin
75
glycosylation that binds to collagen and other proteins in blood vessel walls in the intestinal tissue & will cause tissue injury associated with diabetes (i.e., injuries to the kidneys, blood vessels, peripheral nerves, and the eye lenses
Advanced Glycosylation End Products – AGEs
76
Patho of _______:
Cross-linking and trapping of proteins, albumin, LDL, immunoglobulin, and complement with thickening of the basement membrane or increased permeability in small blood vessels and nerves
Binding to cell receptors (such as macrophages and glomerular mesangial cells) and inducing release of inflammatory cytokines and growth factors that stimulate cellular proliferation in the glomeruli, smooth muscle of blood vessels, and collagen synthesis with fibrosis
Induction of lipid oxidation, oxidative stress, and inflammation
Inactivation of nitric oxide with loss of vasodilation and diminished endothelial function
Procoagulant changes on endothelial cells with promotion of platelet adhesion and reduced fibrinolysis
Advanced Glycosylation End Products – AGEs
77
When tissue do not require insulin for glucose transport (that is they are receiving glucose via Glut 1/2/3, then they are also using the ______ _______ which includes kidneys, RBCs, blood vessels, eye lenses, nerves, and the brain
Polyol Pathway
78
Glucose is converted to ________ and when accumulated it increases intracellular osmotic pressure and attracts water in tissue which causes swelling
sorbitol
79
_____interferes with ion pumps in the nerves and disrupts nerve conduction so that RBCs become swollen and stiff and interfere with perfusion
sorbitol
80
Activation of the polyol pathway reduces ________ (an antioxidant) which contributes to oxidative injury in cells and tissues, particularly blood vessels.
glutathione
81
______ explains:
swelling of the lenses when there is high blood sugar.
cataracts
abnormal nerve conduction
kidney changes (nephropathies of diabetes)***60-70% of all diabetes patients have it
Polyol Pathway
82
Patho of ______ in DM:
AGEs and the increased polyols cause nerve degeneration, delayed conduction, and polyneuropathy
***especially affecting the sensory nerves
Neuropathies
83
Thickening of the capillary basement membrane, endothelial hyperplasia, thrombosis, and pericyte degeneration r/t to glycosylation and polyol pathway and high blood glucose
***characteristic of diabetic microangiopathy
Microvascular Disease
84
______ explains in DM:
retinopathy
nephropathy
neuropathy
Microvascular Disease
85
• Leading cause of blindness worldwide
• Retina is the most metabolically active structure per weight of tissue in the body
o So it is a vulnerable target for neurovascular disease in DM
• Develops more rapidly in Type 2 diabetics
• Diabetics more likely to develop cataracts and glaucoma
• Macular edema (fluid accumulation and retinal thickening near the center of the macula) – leading cause of visual impairment (blurring) among persons with diabetes
• Increased risk of life-threatening systemic vascular complications, including stroke, CAD, and heart failure
• Results from relative hypoxemia, damage to retinal blood vessels and vasoconstriction, RBC and platelet aggregation, influence of vascular endothelial growth factors and growth hormone, and angiogenesis
Retinopathy
86
• Most common cause of CKD & ESRD
• Multiple mechanisms contribute: chronic hyperglycemia, systemic hypertension, hyperperfusion, hyperfiltration, increased blood viscosity, increased glomerular pressure, albuminuria, protein kinase C, growth factors, advanced glycation end products, polyol pathway, inflammatory cytokines, oxidative stress, RAA system, hypercholesterolemia
• Glomeruli are injured by protein denaturation, hyperglycemia with high renal blood flow (hyperfiltration), and intra-glomerular hypertension resistance to glomerular capillary blood flow and decreased glomerular filtration rates (GFRs) microalbuminuria
o Microalbuminuria is the first manifestation of diabetic kidney dysfunction and develops within 5-10 years of disease
Nephropathy
87
* Most common complication of diabetes, affects up to 50% of people with diabetes
* Inflammation, ischemia, oxidative stress, advanced glycation end products, and increased formation of polyol pathways contribute to demyelination, nerve degeneration, and delayed conduction
* Occurs in both somatic and peripheral nerve cells
* Sensory deficits usually precede motor involvement, extremities are involved first (feet then hands)
Neuropathy
88
macrovascular changes are more often seen in DM Type __
1
89
Complication of DM:
Unrelated to severity of DM
Contributing factors include: hyperinsulinemia (insulin resistance), hyperglycemia, hypertriglyceridemia, low levels of HDL, high levels of LDL, lipoprotein oxidation, and platelet abnormalities
Athersclerosis
90
Complication of DM:
more prevalent in persons w/ DM than in persons w/o DM (even in persons with HTN or Hyperlipidemia) – MI and CHF
Most common cause of death for people with DMII
prevalence increases with the duration but not the severity of diabetes
HTN often coexists with DM & increases risk
In type 1- HTN is assoc with development of microalbuminuria
In type 2 – HTN is assoc with metabolic syndrome
Coronary Artery Disease
91
Complication of DM:
twice as common in diabetics than in non-diabetics
more common in diabetic women
ischemic & lacunar strokes are more common
Risk factors: HTN, hyperglycemia, hyperlipidemia, thrombosis, and sleep apnea
Stroke
92
```
____ vascular changes of DM:
Arthersclerosis
Stroke
Coronary Artery Disease
Peripheral Artery Disease
```
macro
93
Complication of DM:
Increased risk with claudication, ulcers, gangrene & amputation in type 2 DM
Occlusions of the small arteries and arterioles, particularly below the knee, cause most of the gangrenous changes of the lower extremities and occur in patchy areas of the feet and toes
Risk factors: age, duration of diabetes, glycemic control, genetics, smoking, hyperlipidemia, HTN
Peripheral Artery/Vascular Disease
94
DM patients are at higher risk for ______ due to imparied senses
infection
95
Why Infection happens in DM:
• Once skin integrity is compromised, tissues’ susceptibility to infection increases as a result of vascular disease & hypoxia.
• Also, Glycosylated Hemoglobin in the RBCs decreases the release of oxygen to tissues
Hypoxia
96
Why Infection happens in DM:
| • proliferate more rapidly in glucose rich environment which provides excellent source of energy
Pathogens
97
Why Infection happens in DM:
| • Decreased d/t vascular changes and autonomic dysfunction, which decreases the supply of WBCs to the affected area
Blood Supply
98
Why Infection happens in DM:
\• Chronic hyperglycemia impairs both innate and adaptive immune responses including:
o abnormal chemotaxis,
o defective phagocytosis,
o inflammatory response to infection is diminished defective phagocytosis
Suppressed Immune Fxn
99
Why Infection happens in DM:
| • Slower collagen synthesis & decreased angiogenesis increase the opportunity for infection
Delayed Wound Healing
100
In Hyperthyroidism (Grave's), labs would show ____ TSH and ____ free T4
low; high
101
TSH comes from ________
anterior pituitary
102
T4 comes from ________
thyroid
103
TRH comes from the _______
hypothalamus
104
anti-TPO tests for _____ in hypothyroid patients
antibodies
105
inflammation of the meninges, membrane that covers brain and spinal cord
meningitis
106
where does pathogen have to go through to get to the meninges?
choiroid plexus
107
mosquito-borne viral infection
encephalitis
108
2 lesions in brain in Alzheimers
neurofibullary tangles
| plaques
109
seizure with stiffening of muscles and may cause one to fall to ground
tonic
110
seizure with single or several jerks
myoclonic
111
seizure with falling down (drop attack)
atonic
112
seizure with jerking of many muscles and sometimes loss of bladder control (grand mal)
tonic-clonic
113
seizure with:
o no change in level of consciousness
o Patient knows what is happening around them
o Motor, sensory, and/or autonomic symptoms present
focal aware (simple seizure)
114
seizure with a change in the level of consciousness
Focal impaired awareness- (complex partial seizure)
