Altered Consciousness Flashcards

(45 cards)

1
Q

Two acute complications of diabetes:

A

Hyperglycemia

Hypoglycemia: blood glucose less than 50 mg/dL

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2
Q

Manifestations of arteriosclerosis in chronic complications of diabetes:

A
Heart: angina and MI
CNS: stroke/CVA
Kidneys: glomerulosclerosis
Lower extremities: gangrene
High blood pressure
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3
Q

Manifestions of microangiopathy in chronic complications of diabetes:

A

Eye: diabetic retinopathy (leading cause of blindness)
Kidney: arteriolar nephrosclerosis
Extremities: gangrene
Neuropathy

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4
Q

Classification of type 1 diabetes:

A
  1. destruction of beta cells of pancreas (autoimmune)
  2. more common in adolescents, usually non obese
  3. circulating and exogenous insulin required
  4. more severe than type 2
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5
Q

Classification of type 2 diabetes:

A
  • genetic interactions regulated by weight, exercise, diet, and stress but is not immune
  • patients endogenous insulin prevents ketoacidosis but does not meet increased needs
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6
Q

3 (triad) symptoms of undiagnosed diabetes:

A
  1. polydipsia (thirst)
  2. polyphagia (appetite)
  3. polyuria (urination)
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7
Q

Important dental considerations for Type 1 diabetic:

A
  1. early appts
  2. normal dietary habits
  3. use a short lasting anesthetic
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8
Q

For a pre-op IV sedation diabetic type 1 patient:

A

Do not eat; hold insulin and schedule early in morning

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9
Q

For a surgical post-op diabetic patient:

A
  1. reduce insulin if food is reduced
  2. check glucose more often
  3. antibiotics for type 1 and 2 if extensive surgical procedure
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10
Q

Clinical SYMPTOMS of hyperglycemia in T1 diabetic:

A
  1. the three polys (polydipsia, polyphagia, polyuria)
  2. weight loss
  3. headache, blurred vision, mental stupor
  4. fatigue to diabetic coma
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11
Q

Clinical SIGNS of hyperglycemia in T1 diabetic:

A

red, hot, and dry face
deep and rapid respirations, rapid heart rate, hypotensive
fruity, sweet breath- diabetic ketoacidosis

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12
Q

Early stage of hypoglycemia:

A
  • difficult conversation, calculations, mood change

- hunger, nausea

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13
Q

Advancing early stage of hypoglycemia:

A
  • skin is cold and wet (hyperglycemia was hot, dry)

- sweating, goosebumps (piloerection), tachycardia, anxiety, resembles intoxication

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14
Q

Late stage of hypoglycemia:

A
  • unconscious due to hypoglycemic come or insulin shock
  • seizures
  • hypotension
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15
Q

Blood glucose normal levels (what level does your brain need and at what level do you exceed renal absorption?):

A

50-150 mg/dl
brain needs 50 mg/dl
above 180 mg/dl, exceeds renal absorption

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16
Q

What occurs when glucose exceeds 180 mg/dl?

A

Glucose is excreted in the urine. It causes the excretion of water, Na, K –> polyuria, polydipsia and dehydration

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17
Q

What occurs in the absence of glucose (or when there’s not insulin to help uptake glucose into cells)?

A

muscle breaks down ketone bodies, acetone is a by-product that causes fruity breath; diabetic ketoacidosis

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18
Q

What happens when ketones exceed proper blood levels?

A

metabolic acidosis (7.3 and below), ketones excreted

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19
Q

What does the body due to compensate for a metabolic acidosis and what are these called?

A
respiratory alkalosis (hyperventilate)
Kussmaul's respirations
20
Q

Management of a hyperglycemic patient:

A

p: Supine
abc: Airway most important
d: Activate EMS, O2

21
Q

Management of conscious, hypoglycemic patient:

A
(patient seems intoxicated)
If conscious:
p: upright
abc:
d: oral glucose (orange juice, soda, candy bar)
patient CAN go home with escort
22
Q

Management of conscious but unresponsive hypoglycemic patient:

A
patient refuses to ingest oral carbs or can't ingest
1. Activate EMS
2a. 50 ml of 50% dextrose IV (ONLY IV)
or 2b. 1 mg glucagon IM or IV
Monitor vitals every 5 mins
3. Discharge with EMS
23
Q

Management of unconscious hypoglycemic patient:

A

p: supine
abc: airway most important, no chest compressions
d: activate EMS
-administer IV 50% dextrose
-IM or IV glucagon
- .5mg of epinephrine (unless they have CV disease)
- decorative icing as last resort
Oral carbs once consciousness is regained, be prepared for hypoglycemic seizures, discharge with EMS

24
Q

What is the end stage of untreated hypothyroidism and what is a drug used to treat hypothyroidism?

A

myxedema coma

Synthroid- L-thyroxine

25
Symptoms of hypothyroidism:
1. parasthesia 2. weakness and fatigue 3. cold intolerance 4. constipation and weight gain
26
Signs of hypothyroidism:
- pseudomyotonic reflex - Hypothermia with dry, scaly skin and puffy eyelids - menorrhagia (abnormal periods) - hoarse voice, thick tongue, slow speech
27
Three types of drugs to be cautious in prescribing to patient with hypothyroidism:
1. Opioid analgesics 2. Sedative-hypnotics 3. Antianxiety
28
Another name for hyperthyroidism:
Graves disease
29
Symptoms of hyperthyroidism:
1. weight loss and weakness 2. nervousness and sweating 3. loose stools 4. heat intolerance (hypo is cold intolerance)
30
Signs of hyperthyroidism:
1. tachycardia, wide pulse pressure 2. fever, warm, moist, soft skin 3. tremor 4. exophthalamos and staring
31
3 treatments for hyperthyroidism:
1. Propylthiouracil 2. subtotal thyroidectomy 3. radioactive iodine ablation of gland
32
characterization of thyroid storm:
1. hyperpyrexia (really high fever) 2. sweating, stupor, coma 3. agitated and disoriented 4. A Fib and tachycardia
33
use of anesthetics in hyperthyroid patient:
anesthetics with vasoconstrictors, but use the least concentrated effective solution and smallest volume; AVOID atropine; contraindicated to use racemic epinephrine for gingival retraction
34
Management of thyroid patients:
``` P -conscious: upright -unconscious: supine ABC D- if patient does not become conscious with positioning, activate EMS, administer O2, vitals, IV infusion ```
35
2 common causes of cerebral infarction (CVA) and two patients at higher risk:
1. Atherosclerosis and thrombosis (81% of CVAs) (embolisms account for 7%) (intracranial hemorrhage 13%) 2. patients with high BP and diabetes mellitus
36
Common sites for embolism:
``` Heart (A. fib, MI, prosthetic and path valves) Neck veins (carotid bifurcation) ```
37
Characterize the two types of intracranial hemorrhages:
1. subarachnoid- w/in subarachnoid space 2. intracerebral- w/in brain parenchyma Occurs most often when BP is elevated
38
two sources of intracranial hemorrhage:
1. ruptured arterial aneurysms | 2. hypertensive vascular disease
39
Predisposing factors for cerebrovascular accident:
1. high BP (greatest risk) 2. diabetes 3. cardiac enlargement 4. hypercholesterolemia 5. smoking 6. history of CVA
40
When can a patient have elective dental treatment following a CV accident?
- after 6 months, but if there is emergency, treat with medications and invasive procedures at hospitals - morning appts, use local with epi with caution, oral or nitrous sedation - be cautious of anticoagulants
41
manifestations of transient ischemic attack:
1/2. abrupt onset but rapid recovery 3. transient numbness and weakness of contralateral extremities ("pins & needles") 4. transient monocular blindness
42
manifestations of infarction:
- gradual onset (TIA is abrupt onset) - TIA precedes - headache limited to side of infarction - paralysis on one side of body (facial asymmetry) (pupils uneven in size) - difficulty breathing, swallowing, unable to speak or slurred speech (aphasia) - loss of bladder/bowel control
43
manifestations of embolism:
-abrupt onset with mild headache before signs and symptoms
44
manifestations of cerebral hemorrhage:
- abrupt onset of signs and symptoms (seconds) - sudden and VIOLENT headache (your brain is bleeding, duh)- localized becoming generalized - nausea and vomiting - chills and sweating - dizziness and vertigo - half of patients lose consciousness
45
management of CV accident (page 12-13)
P: Conscious- upright or semi-supine ABC: BLS as needed Vitals: Elevated BP, pulse rate normal or elevated and bounding; monitor every 5 mins D: Activate EMS, O2, No CNS depressants (so NO nitrous oxide)-- read page 13