2.1 Metabolism Flashcards
1
Q
Endocrine glands: (9)
A
- Pituitary
- Hypothalamus
- Thyroid
- Parathyroid glands
- Thymus
- Adrenal glands
- Pancreas
- Ovary
- Testis
2
Q
What is metabolism
A
-Processes of biochemical reaction in
body’s cells
•Hormones
–Chemical messengers secreted by various glands
3
Q
Pituitary Gland
Location
Function
Parts involved
A
Located in skull beneath hypothalamus • Master gland‖ • Its hormones regulate many body functions •Two parts: – Anterior pituitary –Posterior pituitary
4
Q
Anterior pituitary does what
A
•Several types of endocrine cells •Secretes at least 6 major hormones –Growth hormone –Prolactin –Thyroid-stimulating hormone (TSH) – Adrenocorticotropic hormone (ACTH) –Gonadotropin, follicle-stimulating hormone (FSH) and Luteinizing hormone (LH)
5
Q
Posterior Pituitary does what
A
- Composed of nervous tissue
* Stores and releases antidiuretic hormone (ADH) and oxytocin
6
Q
Thyroid
Location
Parts involved
Function
A
Location –Anterior to upper trachea –Inferior to larynx •Glandular tissue with follicles •Initiated by TSH from anterior pituitary •Secretes hormones –T3, T4 (thyroid hormone) –Calcitonin
7
Q
Parathyroid Glands
A
•4 –6 glands
•Secrete parathyroid hormone (PTH)
–Maintains calcium levels
–Phosphate metabolism
8
Q
Adrenal Glands
Location
Parts
Function
A
•Two pyramid-shaped organs •Sit on top of kidneys •Two organs within each gland – Adrenal medulla – Epinephrine – Norepinephrine – Adrenal cortex – Mineralcorticoids – Glucocorticoids
9
Q
Pancreas
Location
Function
Parts
A
•Behind stomach
–Between spleen and duodenum
•Endocrine gland and exocrine gland
•Endocrine cells produce hormones that regulate carbohydrate metabolism
–Clustered in pancreatic islets (islets of Langerhans)
–4 cell types: alpha, beta, delta, F cells
10
Q
What are hormones?
A
•Chemical messengers secreted by endocrine organs
11
Q
How are hormones transported?
A
•Transported in 4 ways –Endocrine glands –Neurons –Hypothalamus –Paracrine method •Released into bloodstream –Free unbound molecules or –Hormones attached to transport carriers
12
Q
Hormones are controlled by the_______ _______ through ________ & __________ feedback
A
-Pituitary gland
through positive and negative feedback
13
Q
Stimuli for hormone release
A
–Hormonal (hypothalamic hormones stimulate release)
–Humoral (fluctuations in serum levels)
–Neural (nerve fibers stimulate release)
14
Q
What is positive feedback mechanism?
A
Increasing levels of hormones cause another gland to release hormones too.
-Examples include - follicular stage of menstrual cycle and childbirth
15
Q
What is negative feedback mechanism?
A
Sensors in endocrine system detect changes in hormone levels and adjust hormone secretion to maintain homeostasis.
16
Q
Age-related changes
A
•Endocrine system responsible for –Sexual differentiation during fetal development –Stimulating growth and development –Childhood –Adolescence
17
Q
Older age-related changes
Table 18-2 pg. 982 Bob
A
•Pituitary decreases production of ACTH, FSH, TSH •Thyroid decreases in gland activity •Adrenal medulla increases norepinephrine, decreases beta-adrenergic response •Pancreatic blood vessels calcify •Pancreatic ducts distend and dilate •Pancreatic release of insulin –Delayed –Decreased
18
Q
Metabolism alterations -
A
•Disorders of structure and function –Alter normal hormone levels and use –Diabetes mellitus –Obesity –Graves’ disease –Hypothyroidism –Osteoporosis –Cirrhosis
19
Q
Endocrine Assessments
A
- Skin: inspect, palpate
- Nails & hair: texture, distribution, condition
- Facial: symmetry, form, position of eyes
- thyroid gland - enlarged, nodules…
- motor function - deep tendon reflexes
- Sensory function: pain, temperature, touch
- Musculoskeletal: size & proportion of body structure
- Hypocalcemic tetany: Trousseau’s sign or Chvostek’s sign = decreased calcium
20
Q
Hormone diagnostic tests
A
- Serum blood sugar A1c
- T3, T4, TSH
- Individual hormone levels
- Serum electrolytes
- Liver enzymes
- Bilirubin
- Serum albumin
- Serum calcium
21
Q
Pharmacologic interventions for hormone
A
•Goals vary widely •Hormone administered as replacement –Insulin – Antithyroid agents –Thyroid agents –Hormonal agents –Biphosphonates
22
Q
________ is a disorder of hyperglycemia resulting from defects in insulin secretion.
A
Diabetes mellitus
23
Q
What are the 4 major types of diabetes?
A
- DM I
- DM II
- Gestational DM
- Other
24
Q
Pancreas role in hormones (diabetes related)
A
–Alpha cells of the islet cells
-Glucagon
–Beta cells
-Insulin
–Delta cells
-Somatostatin
25
Blood glucose Homeostasis
* Body requires constant supply of glucose
* Not all tissues require resulting insulin
* Normal blood glucose in healthy clients regulated by insulin and glucagon
26
DM I
| Pathophysiology
–Result of pancreatic cell destruction
–Total deficit of circulating insulin
–Autoimmune
–Idiopathic
27
DM I
| Etiology
–Most often occurs in childhood
–Genetic predisposition
–Environmental factors
28
DM I
| Clinical Manifestations
```
–Hyperglycemia
–Breakdown of body fats, proteins
–Development of ketosis
–Polyuria
–Glycosuria
–Polydipsia
–Polyphagia
–Weight loss, malaise, fatigue
```
•Lack of insulin =hyperglycemia
- Glucose cannot enter cell without insulin
- Requires exogenous insulin
29
DM II
| definition
• Adult onset
–Non-insulin-dependent diabetes mellitus (NIDDM)
•Results from insulin resistance
–Defect in compensatory insulin secretion
30
DM II
| Pathophysiology
–Function of insulin impaired by resistance
| –Demand for insulin exceeds supply
31
DM II
| Etiology
•Can occur at any age
–Usually middle age and older
•Major factor is cellular resistance
–Increased by obesity, inactivity, meds, illness, age
32
DM II Risk Factors
* Diabetes in parents or siblings
* Obesity
* Physical inactivity
* Race/ethnicity
* History of gestational diabetes
* Polycystic ovary syndrome
* Hypertension
* Metabolic syndrome
33
Abdominal obesity risk factor for DMII
Men
Women
Men >40"
| Women >35"
34
DM II Clinical Manifestations
```
•Slow onset of manifestations
•Symptoms similar to type 1
•Treatment begins with
–Weight loss
–Increased activity
```
35
Acute complications of Diabetes
–Hyperglycemia
- Diabetic ketoacidosis
- Hyperosmolar hyperglycemic state
- Dawn phenomenon
- Somogyi phenomenon
36
Diabetic Ketoacidosis
about
-involves 4 metabolic problems
-Happens with DM I
- Hyperosmolarity
- Metabolic acidosis
- Extracellular volume depletion
- Electrolyte imbalances from osmotic diuresis
- Increased glucagon levels
37
Somogyi Phenomenon
combo of hypoglycemia during the night with a rebound morning rise in blood glucose to hyperglycemic levels.
38
Diabetic Ketoacidosis Clinical Manifestations
•Manifestations result from severe dehydration, acidosis
–Requires immediate medical attention
–8–10 L fluid to replace losses
–IV fluids with 0.9% NS to 0.45% saline
•Regular insulin used
•Electrolyte imbalance requires monitoring
39
Hyperosmolar Hyperglycemic State (HHS)
```
-Occurs in DM II
•Plasma osmolarity ≥ 340 mOsm/L
•Blood glucose levels > 600 mg/dL
•Serious, life-threatening
•Precipitating factors
•Slow onset
•Results in severe dehydration
```
40
HHS treatment
Treatment
–Correct fluid, electrolyte imbalances
–Lower blood glucose levels with insulin
•Admit to ICU if blood glucose > 700mg/dL
–Establish, maintain ventilation
–Correct shock with adequate IV fluids
–If client is comatose NG suction
–Maintain fluid volume
–Administer insulin to reduce blood glucose
41
Hypoglycemia
Treatment?
Symptoms to watch for?
-low blood sugar
-common in DM I
•15 g of rapid-acting sugar
•Hospitalized if
–Blood glucose <50 mg/dL
• Administer 25
–50% glucose solution
•Glucagon SC, IM or IV
–Coma, seizures
– Altered behaviors
–Caused by sulfonylurea drug
42
Chronic complications of diabetes
- CAD
- HTN
- Stroke
- PVD
- Retinopathy
- Nepthropathy
- Neuropathy
43
Retinopathy
- alterations in blood flow to the retina
- Stage 1 nonproliferative - microaneurysms & edema
- Stage 2: preproliferative - retinal ischemia
- Stage 3: proliferative - possible hemorrhage or retinal detachment
44
Nephropathy
Disease of kidneys - presence of albumin in urine, HTN, edema & progressive renal insufficiency.
45
Diabetic Neuropathy (2 kinds)
Peripheral and visceral neuropathies.
- Thickening of walls of blood vessels
- Decreased nutrients to nerves
- Demyelination of Schwann cells slows nerve conduction
- Formation, accumulation of sorbitol within Schwann cells impairs nerve conduction
46
Visceral neuropathy
```
Autonomic neuropathy.
Ex: - sweating dysfunction
-abnormal pupillary function
-cardiovascular dysfunction
-GI dysfunction
-genitourinary dysfunction
```
47
Peripheral neuropathy
Somatic neuropathy
- polyneuropathy - distal parasthesias
- mononeuropathy - isolate peripheral neuropathy (carpal tunnel)
48
DM Complications involving the feet
- Result of angiopathy, neuropathy, infection
- Vascular changes usually bilateral
- Diabetic neuropathy produces multiple problems
- ----Most common trauma
- Cracks, fissures from dry skin
- Blisters, pressure
- Ingrown toenails
- Begins as superficial ulcer
- Extends deeper
49
Diagnostic tests for diabetes
•Symptoms of diabetes + plasma glucose (PG) > 200mg/dL
–Fasting plasma glucose (FPG) >126 mg/dL
–Two-hour PG > 200 mg/dL
-oral glucose tolerance test (OGTT)
•Following levels for FPG:
–Normal FG: 100 mg/dL
–Impaired FG: > 100 < 126 mg/dL
50
Prediabetes levels
–100 – 126 mg/dL
| At increased risk of developing diabetes
51
Fasting blood glucose range
70 –110 mg/dL
52
Insulin lispro (Humalog)
- Human insulin analog
- derived from genetically altered E. coli
- Rapid-acting or Ultra-short insulin.
- Rapid onset (<15 min)
- Peak (30-60 min)
- duration (3-4 hrs)
53
Regular insulin
- unmodified crystalline insulin
- short-acting insulin
- also used to treat DKA
- clear
- ONLY insulin that may be given IV
- onset 30 min - 1hr
- peak 2-3 hrs
- duration 4-6 hrs
54
Insulin glargine (Lantus)
- 24 hour long-acting rDNA human insulin analog
- sub Q qd at bedtime
- Used for DM I & DM II
- No peak time
55
Which insulin can be administered through an IV?
Regular Insulin
56
How is insulin dispensed?
-100unit/mL (U-100)
or
-500unit/mL (U-500)
57
When would U-500 insulin be used?
- In rare cases of insulin resistance when clients require very large doses.
- requires perscription
58
DM II clients receive what kind of diabetic medication in the hospital?
- parenteral
| - NO oral medications for diabetes is administered in the hospital due to the slow response of the meds.
59
Which insulin injection sites have the most rapid absorption?
```
#1 Abdomen
#2 Deltoid
#3 Thigh
#4 Hip
```
60
Don'ts of administration of a insulin injection:
- Don't Rub/massage injection site
| - Don't inject into an area to be exercised
61
Lipodystrophy (or lipoatrophy)
- atrophy of subcutaneous tissue
- Hardened tissue, may have orange-peel texture, at injection site that is overused.
- happens more with pork and beef insulins
- refrigerated insulin may also trigger
62
DM II Hypoglycemic agents
- used to stimulate/increase insulin secretion
- prevents breakdown of glycogen to glucose in liver
- increases peripheral uptake of glucose
63
Exenatide (Byetta)
- only injectable hypoglycemic
- signals pancreas to make insulin
- stops liver conversion of glycogen to glucose
- decreases absorption of sugar from intestines.
64
Recommended carbohydrate intake
45-65% of daily diet
–Plant foods, milk, some dairy
–Sucrose substituted for other carbohydrates
65
Recommended protein intake
15-20% of daily diet
–Low in fat, cholesterol
–Lower than most people consume
66
Recommended Dietary Fats
–Less than 10% saturated fat total kcal/day
–Cholesterol <300mg/day
- Saturated fat (meat, butter, lard)
- Polyunsaturated (oils)
- Monosaturated (olive oil)
67
Diabetic diet plan
```
–Restrict refined sugars
–Nutritive sweeteners with caution
–Alcohol consumption
-Signs of intoxication and hypoglycemia similar
-Light beer recommended alcoholic drink
```
