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Patho > Endocrine Disorders and Allergic Reactions > Flashcards

Endocrine Disorders and Allergic Reactions Flashcards

1
Q

What is glucose?

A

The primary source of fuel for the majority of our body’s cells - when metabolized with oxygen (aerobic metabolism) it produces CO2 and H2O as byproducts

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2
Q

Why does the brain require continuous glucose supply?

A

it does not synthesize or store its own

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3
Q

What is a normal blood glucose level in non diabetics?

A

fasting blood glucose is around 4.4 - 5.0mmol/L
following a meal, this may rise to 5.5 - 6.7mmol/L

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4
Q

What is insulin?

A

-released by the B cells in the pancreatic islets when higher levels of glucose are detected in the blood
-insulin facilitates the entry of glucose into body cells to be used in metabolic processes

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5
Q

What is Glycogenolysis?

A

the breakdown of glycogen into glucose

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6
Q

What is Gluconeogenesis?

A

the synthesis of glucose from amino acids, glycerol, and lactic acid -can then be released or stored (as glycogen)

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7
Q

What is Glycogenesis?

A

the formation of glycogen from glucose

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8
Q

What is fat metabolism?

A

-Fat is the densest form of fuel storage
-The metabolism of triglycerides yields a glycerol molecule and three fatty acids
-Glycerol can either be used to produce energy or to produce glucose
-Fatty acids can be used by many body tissues as a source of energy
-When fatty acids are used for energy, they release ketones into the blood as a byproduct

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9
Q

What is protein metabolism?

A

-Excess amino acids are converted to fatty acids, ketones or glucose - very minimal storage of amino acids
-When metabolic glucose needs are higher than glucose intake, the body may need to break down proteins and use the amino acids to synthesize glucose (Gluconeogenesis)

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10
Q

What does insulin do?

A

-Promotes glucose uptake by target cells
-Promotes glycogenesis and converting excess glucose to fat
-Inhibits glycogenolysis and fat breakdown
-Inhibits gluconeogenesis and increases protein synthesis
-Insulin binds to insulin receptors on the plasma membrane of a target cell
-This triggers a process that essentially opens a gateway to allow glucose to enter the cell

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11
Q

What does glucagon do?

A

-Secreted by the alpha cells of the islet to raise blood sugar
-Regulates BGL between meals, during fasting, and during periods of increased metabolic demand (exercise)
-Travels to the liver to initiate hepatic breakdown of glycogen (glycogenolysis)
-Increases amino acid transport to the liver to synthesize glucose and stimulates protein conversion to glucose (gluconeogenesis

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12
Q

What does somatostatin do?

A

-Secreted by delta cells of the islet to inhibit secretion of insulin and glucagon by the beta
and alpha cells
-Several triggers exist for its release, but the purpose is to increase the time in which
nutrients are available in the blood for use by body cells

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13
Q

What does epinephrine do?

A

Stimulates glycogenolysis and inhibits insulin secretion

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14
Q

What does growth hormone do?

A

Increased protein synthesis, release of fatty acid

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15
Q

What is diabetes mellitus?

A

A group of metabolic disorders characterized by hyperglycemia resulting from an imbalance
between insulin secretion and cellular responsiveness to insulin

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16
Q

What are the 4 different types of diabetes?

A

-Type 1
-Type 2
-Gestational
-Diabetes due to other causes

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17
Q

What is prediabetes?

A

-A diagnostic term used when blood glucose is elevated but does not yet meet the
threshold criteria for diagnosis of DM
-This is more common in patients at risk for developing Type 2 DM
-Drastic lifestyle modifications can alter progression and ultimately prevent diabetes

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18
Q

What percent of DM cases are Type 1?

A

Approximately 5%

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19
Q

What is type 1 diabetes?

A

-most often occurs in childhood - can develop at any age (rare)
-characterized by destruction of the pancreatic beta cells, often manifests rapidly
-complete lack of insulin results in hyperglycemia and a breakdown of body fats and proteins - leading to ketone buildup and ketoacidosis
-All patients with type 1 diabetes require exogenous insulin
-Often referred to as insulin dependent diabetes mellitus (IDDM)

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20
Q

What are the 3 most common initial manifestations of type 1 diabetes?

A

The 3 Polys
-Polyuria (excessive urination)
-Polydipsia (excessive thirst)
-Polyphagia (excessive hunger)

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21
Q

What are other common initial manifestations of type 1 diabetes?

A

abdominal pain, nausea, vomiting, somnolence and general malaise (from ketoacidosis)

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22
Q

What is type 2 diabetes?

A

-Accounts for most cases of DM (90-95%)
-Sometimes referred to as adult-onset diabetes, but it is becoming a more common occurrence in overweight children/adolescents
-Characterized by a relative insulin deficiency with or without complete destruction of beta
cells
-While there is a strong genetic influence on developing type 2 diabetes, it is mostly caused by chronically poor diet and lack of self-care

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23
Q

What are the metabolic abnormalities associated with type 2 diabetes?

A

-Insulin resistance
-Altered insulin secretion
-Increased glucose production

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24
Q

What is insulin resistance and what causes it?

A

-The decreased ability of insulin to act effectively on target tissues
-Obesity and poor diet lead to an inadequate response to insulin
-Excessive adipose tissue is poorly perfused which leads to cell damage/necrosis and a chronic systemic inflammatory response
-Adipose tissue becomes resistant to insulin (glucose cant enter the cell) which worsens the hyperglycemia and stimulates the beta cells to produce even more insulin
-Overuse of insulin receptors due to overproduction of insulin also contributes to
the resistance

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25
Q

What is altered insulin secretion?

A

-Poor dietary intake (high sugar content) leads to an increased secretion of insulin by the beta cells to maintain normal BGL
-In time, this increased secretion leads to beta-cell exhaustion and failure
-Worsens hyperglycemia

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26
Q

What causes excess glucose production in type 2 diabetes?

A

-Insulin resistance in hepatic (liver) cells triggers glycogenolysis and gluconeogenesis
-Worsens hyperglycemia

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27
Q

Does type 2 diabetes require exogenous insulin?

A

-Initially, T2DM does not require treatment with exogenous insulin because they do not have an absolute lack of insulin, just inefficient insulin function and a relative lack of
insulin
-These patients are started on a variety of oral hypoglycemics
-As the disease progresses, and the beta cells begin to fail from overuse, advanced cases of T2DM may require exogenous insulin

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28
Q

What are some of the comorbidities of type 2 diabetes?

A

-As insulin resistance worsens, it causes a decrease in endothelial secretion of NO, a potent vasodilator
-Leads to vasoconstriction and increased vascular
resistance
-Insulin normally inhibits lipolysis (breakdown of fats) but the insulin resistance promotes lipolysis which leads to an increase in blood lipids
-Patient at very high risk for: Dyslipidemia, Hypertension, Abnormal coagulation, Atherosclerosis, Heart disease

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29
Q

What us Gestational Diabetes (GDM)?

A

-Characterized by any degree of glucose intolerance that occurs during pregnancy (usually 2nd and 3rd trimester)
-Careful monitoring and treatment are essential because GDM patients are at higher risk for complications, mortality and fetal abnormalities
-Increased Risk of developing type 2 DM so they must be monitored and maintain a healthy lifestyle to prevent its development

30
Q

What is diabetes due to other causes?

A

-Very small percentage of DM cases where the etiology doesn’t fit into one of the other three scenarios
-Pancreatic disease/removal of pancreatic tissue
-Endocrine diseases

31
Q

What causes Polyuria (excessive urination)?

A

-Hyperglycemia leads to increase glucose loss in the urine
-Since glucose is a highly osmotically active molecule, it “pulls” a large volume of H2O with it into the urine

32
Q

What causes Polydipsia (excessive thirst)?

A

Hyperglycemia enacts an osmotic “pull” on the cytosol which leads to cellular dehydration that triggers the thirst center in the hypothalamus

33
Q

What causes Polyphagia (excessive hunger)?

A

results from cellular starvation and the depletion of cellular stores of carbohydrates, fats and proteins

34
Q

What are the signs and symptoms of diabetes?

A

-Weight loss, despite normal or increased appetite is common in T1DM
-Loss of body fluids from osmotic diuresis
-Lack of insulin forces the body to metabolize fat stores and cellular proteins for energy
-Ketoacidosis induces vomiting which contributes to volume loss
-Blurred vision - hyperosmolar fluids in the eye
-Fatigue - low plasma volume
-Skin infections - chronic systemic inflammatory response (T2DM)

35
Q

What are the 3 major acute complications of DM?

A

-Diabetic Ketoacidosis
-Hyperosmolar Hyperglycemic State (HHS)
-Hypoglycemia

36
Q

What is diabetic ketoacidosis?

A

-Most common in patients with T1DM
-Lack of endogenous insulin leads to increased release of fatty acids from adipose tissue (breakdown of triglycerides into FA and glycerol)
-When fatty acids are used as energy, they produce ketones as a byproduct
-As ketones build up in the blood stream, the patient may develop a metabolic acidosis
(ketosis/ketoacidosis)
-This is a common initial presentation of undiagnosed diabetics

37
Q

What are the clinical manifestations of diabetic ketoacidosis?

A

-Building up to the DKA: three “polys”, nausea, vomiting, abdominal pain and progressive fatigue
-LOA will gradually decline from fully alert, to confusion, stupor and eventually coma
-Keto acids have a distinct fruity smell which presents itself on the patient’s breath
-Tachycardia - decreased blood volume
- Increased rate and depth of breathing - mitigate the acidosis
-Kussmaul respirations - deep, gasping respiration

38
Q

What is Hyperosmolar Hyperglycemic State (HHS)?

A

-Similar to DKA but does not involve ketoacidosis
-More common in T2DM
-Characterized by: Hyperglycemia, Hyperosmolarity causing dehydration, Altered LOA
-Relative insulin deficiency in T2DM causes reduced glucose utilization resulting in increased glucagon release and glucose output by the liver
-Leads to hyperglycemia and resultant osmotic water loss
-Decreased blood volume leads to a lower glomerular filtration rate and therefore less glucose eliminated in the urine – further worsens the hyperglycemia (snowball effect)

39
Q

What are the clinical manifestations of HHS?

A

-Weakness, dehydration, initial polyuria, and polydipsia are common symptoms of HHS
-Neurological deficits include hemiparesis, seizures and coma caused by the osmotic diuresis of brain cell

40
Q

What is hypoglycemia?

A

-Hypoglycemia is any condition resulting in a BGL < 4.0mmol/L, with or without symptoms (< 3.0 for pts < 2yrs old)
-Most commonly occurs in IDDM due to improper regulation of BGL
Etiology and Pathogenesis:
-Error in insulin dose
-Failure to eat while maintaining regular
-Insulin dose
-Increased exercise
-Post sympathetic response
-Medication changes
-Dietary changes
-Alcohol use (decreases gluconeogenesis)

41
Q

What are the clinical manifestations of hypoglycemia?

A

Most symptoms are caused by the decrease glucose uptake in the brain:
-Headache
-Confusion
-Bizarre behaviors
-Seizure
-Coma
Sympathetic nervous system response induces:
-Anxiety
-Tachycardia
-Diaphoresis (++)
-Vasoconstriction of skin vessels (pale, cool and clammy)
-Many of the S&S can easily be misinterpreted as intoxication

42
Q

What are some of the chronic complications of diabetes?

A

-Microvascular Complications
-Macrovascular Complications
-Foot Ulcers and Infections

43
Q

What are the microvascular complications?

A

Diabetics tend to have varying degrees of endothelial dysfunction leading to:
-Neuropathy - peripheral nerve dysfunction causing numbness or weakness
-Retinopathy - damage to the retina leading to potential vision problems
-Nephropathy - kidney disease
-GI motility disorders - spasms or lack of motion in the GI tract

44
Q

What are the macrovascular complications?

A

-Coronary Artery Disease (CAD) - heart attacks, angina, heart failure
-Cerebral Vascular Accident (CVA) - stroke
-Peripheral Vascular Disease – HTN

45
Q

Why do diabetics get foot ulcers?

A

-The neuropathy and vascular inefficiency can lead to ulcers in the feet
-Complicated by a decreased peripheral pain sensation leading to ignoring of a buildup of minor traumas, altered gait with increased pressures, and poorly mobilized inflammatory efforts
-Diabetics have a weakened inflammatory and immune response due to hyperglycemia and vascular compromise. This leads them more susceptible to infections (minor and major)
-Common for poorly controlled diabetics to have toe or foot amputations due to significant infections

46
Q

What are the clinical manifestations of hyponatremia (Na+ < 135mEq/L)?

A

-Decreased concentration of Na+ will lower the ECF osmolarity, drawing fluid into the cells (hypotonic hyponatremia)
-Muscle cramps, weakness, fatigue
-Abdominal cramps, nausea, vomiting, diarrhea
-Seizures, coma, altered LOA

47
Q

What are the clinical manifestations of hypernatremia (Na+ > 145mEq/L)

A

-Due to ECF water loss and cellular dehydration (increased osmolarity of ECF “pulls” water from the cells)
S&S:
-Thirst, decreased urine
-Warm, flushed skin
-Rapid, thready pulse
-Decreased BP
-Dry skin/mucous membranes
-Decrease salivation/lacrimation
-Dry/sticky mouth, difficulty swallowing
-CNS - HA, agitation, seizure, coma

48
Q

What are the clinical manifestations of Hypokalemia (K+ < 3.5mEq/L)?

A

-Reflects both the intracellular functions of potassium and the body’s attempt to regulate the narrow ECF range
S&S:
-Increased urine output
-Anorexia, nausea, vomiting
-Constipation, abdo distention
-Hypotension
-ECG (long PR, ST depression, flattened/inverted T-waves, U-wave)
-Weakness, fatigue, muscle cramps

49
Q

What are the clinical manifestations of Hyperkalemia (K+ > 5.0mEq/L)?

A

-Muscle weakness, shortness of breath (respiratory muscle weakness)
-ECG changes (peaked/narrow T waves, widened QR complex)
-Eventually PR interval lengthens and T wave disappears
-Bradycardia and eventual ventricular fibrillation
-The faster the onset of hyperkalemia, the more severe the manifestations

50
Q

What is hypersensitivity?

A

an abnormal and excessive response of the activated immune system that causes injury and damage to host tissues

51
Q

What are IgE mediated reactions?

A

-IgE mediated reactions that develops rapidly upon exposure to an antigen (allergen)
-Many allergens exist that can produce this reaction: Pollen, Dust, Animal dander, Medications, Foods, Household chemicals, etc.
-Exposure to an allergen can by through: Inhalation, Ingestion, Absorption (skin), Injection, etc.
-Depending on the entry mechanism, the reaction may be localized or systemic

52
Q

What cells are involved in IgE mediated reactions?

A

-T2H cells
-Mast cells
-Basophils

53
Q

What do T2H cells do in allergic reactions?

A

T2H cells direct B cells to produce IgE antibodies

54
Q

What do mast cells and basophils do in allergic reactions?

A

-Mast cells, and basophils are granulocytes (contain granules rich in chemical mediators like histamine)
-Mast cells - connective tissues
-Basophils - bloodstream
-Mast cells are in higher concentration in tissues more likely to come in contact with an allergen - respiratory tract, GI/GU tract, adjacent to blood and lymph vessels

55
Q

What occurs at the initial exposure to an allergen?

A

-T2H direct B-cells to produce allergen-specific IgE
antibodies in the plasma membranes of mast cells and basophils
-During subsequent exposures to the same allergen, the IgE antibodies stimulate mast cell
degranulation and release of vasoactive mediators

56
Q

What are the two phases of type 1 hypersensitivity reactions?

A

Primary and secondary

57
Q

What occurs in the primary phase of a reaction?

A

[vasodilation, vascular leakage, smooth muscle contraction]
-Usually occurs within 5-30 minutes of an exposure
-Mast cell degranulation causes release of many chemical mediators; primarily histamine
-Histamine acts by increasing nitric oxide (NO) production which induces vascular smooth muscle relaxation (vasodilation)
-It also increases the permeability of micro vessels (fluid leak - edema) and causes bronchoconstriction (wheezes)

58
Q

What occurs in the secondary phase of a reaction?

A

[infiltration of more inflammatory cells (eosinophils) and epithelial cell damage]
-Occurs 2-8 hours after primary phase and can last for several days
-Part of the normal inflammatory response triggered by mast cell degranulation
-A chemical process occurs which results in the release of leukotrienes and prostaglandins, effects are similar to those of histamine, but they tend to last longer
-Eosinophils and leukocytes are also attracted to the site contributing to the inflammatory
response

59
Q

What is anaphylaxis?

A

-A systemic and life-threatening IgE mediated hypersensitivity reaction caused by the widespread release of histamine into the bloodstream
-Results in massive vasodilation (hypotension), arterial hypoxia, and airway edema

60
Q

What is the severity of a reaction dependent on?

A

The degree of preexisting sensitization NOT the quantity of allergen

61
Q

What are the signs and symptoms of anaphylaxis?

A

-Erythema (redness) and urticaria (hives) - localized or widespread
-Hypotension (vasodilation), tachycardia (compensatory)
-GI disturbances - nausea, vomiting, diarrhea, abdominal cramping
-GI mucosal edema, smooth muscle constriction
-Dyspnea, wheezing, tightness in the throat, decreased SpO2, bronchoconstriction
-Cardiac arrhythmias, airway edema (angioedema)

62
Q

What are the locations of the different adrenergic receptors?

A

-Alpha 1 (α1) - smooth muscle in blood vessels, sphincters, iris
-Alpha 2 (α2) - cardiac muscle, platelets in blood
-Beta 1 (β1) - cardiac muscle, posterior pituitary, juxtaglomerular cells
-Beta 2 (β2) - smooth muscle in airways, smooth muscle in cardiac BV

63
Q

What do a1 receptors do?

A

α1 - peripheral vasoconstriction (increased BP)

64
Q

What do a2 receptors do?

A

α2 - coronary artery dilation (increased myocardial blood supply)

65
Q

What do β1 receptors do?

A

β1 - increased chronotropic, dromotropic, inotropic

66
Q

What do β2 receptors do?

A

β2 - bronchodilation

67
Q

What is anaphylactic shock?

A

-Anaphylactic shock is a form of distributive shock
-Loss of blood vessel tone, enlargement of the vascular compartment, and displacement of
vascular volume away from the heart
-The volume of blood remains the same, but the container size increases and is therefore
inefficient to perfuse tissue
-Anaphylactic shock occurs when the symptoms of anaphylaxis progress to the point where
the brain and vital organs are not being perfused

68
Q

What is an anaphylactoid reaction?

A

-An immediate systemic reaction that mimics anaphylaxis but is not mediated by IgE immunity
-Anaphylactoid reactions are either triggered by the complement system or bradykinins (peptides) which result in direct activation of mast cells and/or basophils
-The end result is the same and should be treated no differently from anaphylaxis

69
Q

What is a local allergic reaction?

A

A localized hypersensitivity reaction that usually occurs when the allergen is confined to the
exposure site

70
Q

What are common local allergic reaction symptoms?

A

-Urticaria
-Allergic rhinitis
-Dermatitis
-Mild angio edema
-Occasionally bronchial asthma

Patho (9 decks)

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