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Cardiopulmonary > Final Study Guide > Flashcards

Final Study Guide Flashcards

1
Q

4 Types of cells found in pancreas

A
  1. Alpha Cells
  2. Beta Cells
  3. Delta Cells
  4. F or PP cells
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2
Q

What Alpha Cells Release

A

Produce glucagon

Stimulated by hypoglycemia

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3
Q

What Beta cells release

A

produce insulin

when high blood glucose

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4
Q

What delta cells release

A
  • peptide hormones somatostatin

- inhibit release of glucagon and insulin

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5
Q

What F or PP cells release

A

Secrete pancreatic polypeptide hormone (appetite)

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6
Q

Type I Typical Characteristics

A
  • Juvenile
  • insulin-dependent DM, from beta cell destruction leading to an absolute insulin deficiency
  • 5-10%
  • Sudden onset
  • mostly in children
  • thin/normal body
  • ketoacidosis
  • autoantibodies
  • low endogenous insulin
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7
Q

Type II Typical Characteristics

A
  • Adult onset
  • non insulin dependent
  • from progressive insulin secretory defect on background of insulin resistance
  • 90-95% of pop
  • gradual onset
  • mostly adults
  • obese
  • RARE ketoacidosis
  • NO autoantibodies
  • Normal endogenous insulin
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8
Q

Late autoimmune diabetes in adults

A
  • Slow onset Type 1
  • some disease-associated autoantibodies
  • NO insulin requirement at time of diagnosis
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9
Q

Type 1 DM Pathologic Process

A

Beta cell destruction which can’t make insulin

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10
Q

Type 2 DM Pathologic Process

A

Cellular resistance to insulin

  • increase with obesity
  • insulin resistance hyperinsulineamia impaired glucose tolerance
  • impaired fasting glucose-hypoglycemia-EARLY DM-beta cell failure and requires insulin like type 1
  • Decreased beta cell responsiveness to plasma glucose levels, abnormal glucagon secretion, islet dysfunction-decreased beta cell mass, abnormal beta function, alterations in the insulin receptor of muscle liver and adipose
  • Amyloid formation in pancreas with islet cell destruction
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11
Q

Classic symptoms of Type 1 DM

A 
Lethargy 
stupor
breath smell acetone weight loss
Kussmaul breathing (hyperventilation)
nausea
vomit
abdominal pain
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12
Q

Classic symptoms of DM

A 
Polydipsia
plyphagia
blurred vision
polyuria
glycosuria
paresthesias
recurrent infection
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13
Q

Acute complications of DM

A 
-Hypoglycemia 
pallor
tremor
balance
fatigue
confused
dizzy
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14
Q

Diabetic Ketoacidosis Symptoms

A

Decreased insulin
more stress hormones
more glucose production
more ketones=odor

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15
Q

Chronic DM Symptoms

A 
Microvascular disease
-neuropathy
-retinopathy
-nephropathy
Macrovascular disease
-atherosclerosis
-CAD
-Stroke
-PVD
Cardiovascular disease
nephropathy
retinopathy
neuropathic ulcer
Decrease awareness
decrease blood for healing
increased glucose in body fluid
decreased WBCs 
poor function of WBC
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16
Q

Tri-Neuropathy

A
  1. Sensory
  2. Motor
  3. Autonomic
17
Q

Sensory Neuropathy Loss

A

Cannot sense
Type 2: stocking glove
Type 1: Small nerve fibers

18
Q

Motor neuropathy

A 
Loss intrinsics foot muscles
claw toe deformity
high peak pressure
no ankle her reflex 
Type 1: large nerve fiber damage
19
Q

Autonomic Neuropathy

A

Nonelastic
Dry skin
No sweat or oil production
Type 1: large nerve fibers and sympathetic ganglion

20
Q

Neuropathic Ulcer

A 
Plantar surface
toes
bony prominence
pale pink or red
periwound callus/hyperkeratotic
minimal drainage
round 
may not have pain
pulse may be normal 
diminished or bounding infection
21
Q

How advanced glycated end products are formed

A

Chronic complication of DM which his result from attachment of glucose metabolites onto proteins
results in irreversible cross links with collagen

22
Q

Consequences of overproduction of glycated endproducts

A

Inelasticicty of ROM deficits in foot, high peak pressure, gait abnormalities
-Can lead to nephropathy

23
Q

Stage of Inflammation: Hemostasis

A

Time: 30min
Fibrin formation–lysed by PLASMIN
Endothelial cells release PROSTACYCLIN (arteriole vasodilator to bring healing cells)

24
Q

Stage of Inflammation:

Inflammation

A

Time: 3-7day
Invasive of neurophils that lyse nonviable cell components
Platelets and Neutrophils release Growth Factors,

Eosinophils phagocytose devitalized tissue

Mast cells and Basophils–release histamine (increases vascular permeability and attract Monocytes)

Monocytes–>macrophages

Lymphocytes produce Antibodies for immune response

25
Q

Stage of Inflammation: Proliferation

A

Granulation Tissue
Fibroblasts–>collagen, CT, GF

Endothelial cells–>new capillaries and transport O2 and nutrients to wound

Macrophages secrete GF

Myofibroblasts–>fibronectin, collagen, GAGs, enzymes, encourage wound contraction

Platelets and Fibroblasts–>fibronectin

Platelets macrophages–>GF, (PDGF, TGF-B), Keratinocytes initiate wound coverage at edges
Epithelial cells cover wound surface, basal cells, and basement membrane bond granulation tissue and epidermal cells

26
Q

Stage of Inflammation: Remodeling

A

Fibroblasts–>collagen

Epithelial cells, macrophages, fibrobalsts, leukocytes–>collagenase

Tissue refines to accommodate function

Skin return to original color

27
Q

Differentiate partial from full-thickness wounds

A

Partial thickness: loss of epidermis and part of the dermis. heals at 1mm/day epithelial cells migrate across wound surface. originates at the wound margins, hair follicles, and sweat ducts.

Full thickness: loss of all of the dermis and into subcutaneous tissue

28
Q

Approaches to wound healing

A

Primary Intension: Edges brought together and sutured, stapled, bonded

Secondary Intention: for large tissue when use other material to bring about closure

Third: Retaining sutures prevent large opening. drains prevent edematous dehiscence

29
Q

Transcutaneous oxygen tension in Pt Values

A

Non invasive measurement of healing
Normal: >40mmHg
Delayed: <20mmHg

30
Q

Venous Ulcers Characteristics

A 
Heavy legs
ache
spider veins
varicose
edema
skin changes
ulceration
skin hyper pigment
hemosiderin
lipodermatosclerosis
dilated long saphenous vein 
strophie blanche
dermatitis 
thick skin
cellulitis 
Gaiter area
31
Q

Venous Ulcers Causes

A 
DVT
Surgery
Ankle hypo mob or fusion
Excessive standing 
morbid obesity
pregnancy
CHF
32
Q

Semmes-Weinstein monofilaments

A 
Normal: 3.61
Neuropathy present: 4.17
Loss of protective sensation:  5.07
Loss of sensation: 6.10
Test: great toe, medial malleolus, tibial tuberosity
33
Q

General Identifying Characteristics of Chronic Venous Insufficiency

A

Increased vein circumference
poolin gin distal extremity
vessel dilation and elongation
increased collagen deposition in B vein walls and skin, plasma protein leaks into interstitial space with resulting fibrin cuff around arterioles
increased leukocytes with decrease immune function
increased inflammatory cells resulting n tissue remodeling and dermal fibrosis
Varicose veins, edema without ulceration, skin changes with or without ulceration

34
Q

Skin changes in diagnosis CVI

A 
Hyperpigmentation
lipodermatosclerosis
dilated long saphenous vein 
atrophie blanche 
edema
dermatitis
thickened skin
cellulitis 
Gaiter area

Cardiopulmonary (2 decks)

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